components of the lymphatic system are lymph, lymphatic vessels, lymphoid cells (lymphocytes and

other cells), primary lymphoid tissues and organs (red bone marrow and the thymus), and secondary
lymphoid tissues and organs (lymph nodes, tonsils, MALT, the appendix, and the spleen).

Answer: Immunity is the body’s ability to resist infectious organisms or other substances that could
damage tissues and organs. Resistance is the ability of the body to maintain its immunity.

What are the two major ways that the body carries out the immune response
against a specific antigen?
Direct attack by T cells and attack by circulating antibodies
 
When any of your body cells becomes infected with a pathogen, to what protein do
the foreign peptides become attached that initiates the immune response?
Class I MHC proteins

A
Abnormal peptides
Abnormal peptides in the cytoplasm of a cell can become attached to MHC (major
histocompatibility complex) proteins and then be displayed on the surface of the cell’s
plasma membrane. The recognition of such displayed peptides by T cells can initiate an
immune response.
Abscess
This viscous fluid mixture is known as pus. An accumulation of pus in an enclosed tissue
space is called an abscess.

active immunity
immunity developed from an individual’s own immune system, AFTER exposure to antigen
Active immunity- Develops in response to antigen exposure
Active immunity
• Naturally acquired
• Develops after natural exposure to antigens in the environment
• Example: contracting the measles gives immunity against future infection by that
specific pathogen
• Artificially induced
• Develops after administration of an antigen
• Example: vaccination (immunization)
• Vaccines contain dead or inactive pathogens, antigens derived from those
pathogens, or simulated antigens
• Stimulate immune response to produce antibodies against that specific
pathogen

acute inflammation
inflammation occurring for a limited time period; rapidly developing

Adaptive (specific) immunity

1
 When an antigen appears, the adaptive immune system response begins with
the activation of specific T cells and B cells
Adaptive (Specific) Immunity. In contrast, two classes of lymphocytes, T cells and B cells, respond to specific antigens. If a bacterial
pathogen invades peripheral tissues, these lymphocytes organize a defense against that particular type of bacterium, but NOT other
bacteria and viruses. More importantly, this type of immunity also protects us against further attacks by the same type of pathogen.
For this reason, we say that T cells and B cells provide an adaptive defense. Many specific defenses develop after birth as a result of
accidental or deliberate exposure to antigens. Adaptive (specific) immunity depends on the activities of specific lymphocytes—B
cells and T cells.

• Coordinated and produced by T cells and B cells

• Not present at birth
• Acquired by:
• Exposure to antigen
• Active immunity
• Receiving antibodies
• Passive immunity
Adaptive Immunity:
• Uses lymphocytes, APCs, and specific molecules to identify and destroy non-self substances
• Depends upon the ability of its cells to
• Recognize antigens by binding to them
• Communicate with one another so that the whole system mounts a specific response
relatively slow but very specific and effective immune response controlled by lymphocytes
Properties of adaptive immunity

1. Specificity

• T cells and B cells have receptors for only one specific antigen
• Responses of activated T cell or B cell are also specific (do not affect any other antigens)
2. Versatility
• Millions of lymphocytes, each sensitive to a different antigen
• When activated, a lymphocyte divides
• Produces more lymphocytes with same specificity

Our immune system’s ability to attack and defend us from any antigen at any time is a property of
adaptive immunity called versatility

•
3. Immunologic memory
• Activated lymphocytes produce two groups of cells
• Groups that attack invaders immediately
• Group that remains inactive unless exposed to the same antigen later
• These memory cells “remember” antigens, making future attacks
faster, stronger, and longer-lasting
 
What property of adaptive immunity allows a person to have the chicken pox when he or she
is six years old and still be immune to chicken pox at age 45? MEMORY
•
4. Tolerance
• Immune response ignores “self” but targets abnormal and foreign “non-self” cells and
toxins
• Can develop over time in response to chronic exposure to an antigen

2
 While our immune system is fully prepared to fight foreign antigens, our T cells
and B cells normally do not attack self-antigens. What is this property of adaptive
immunity called? tolerance

The intentional introduction of antigenic materials into the body is called

The intentional introduction of antigenic materials into the body is

called artificially acquired active immunity. This is termed “artificially induced,”
because the introduction of an antigen into the tissues is through deliberate action,
usually in the form of a vaccine. If exposure happened through chance
environmental encounters, the exposure would be termed “naturally acquired
active immunity.” The phrase “active immunity” underscores the fact that the
body needs to produce an antibody in order to mount an immune response. This is
in contrast to passive immunity, in which the body acquires a preformed antibody
or other factors that were produced outside the body.

When a person is bitten by a rabid dog, by what means do medical personnel attempt to prevent
infection by the rabies virus?
Artificially acquired passive immunity

What type of immunity is conferred when a baby receives antibodies from her mother?
Because the baby is being given antibodies, this is passive immunity. This is, of course, a natural way
of conferring antibodies. Antibodies cross the placenta or are given through the milk in breastfeeding.
So this is naturally acquired passive immunity.

Which type of immunity develops as a result of natural exposure to an antigen in the environment?
Naturally acquired active immunity is the type of immunity which develops as a result of natural
exposure to an antigen in the environment. “Naturally acquired” indicates that antigen is encountered
in the course of normal environmental interaction. The phrase “active immunity” indicates that
antibody is actively being made by a person after an antigen is processed by the immune system.

Innate (nonspecific) immunity is a type of body defense that you are born with and does not
distinguish among different threats. Adaptive (specific) immunity is acquired after birth and
after exposure to a particular antigen.

Adreneal gland
One of the stress related hormones produced by the highlighted gland is cortisol produced in the
cortex

afferent lymphatic vessels

lead into a lymph node
AFFERENT lymphatic vessels transport lymph to a lymph node, whereas EFFERENT lymphatic
vessels carry lymph away from a lymph node.

aging on the immune system

A decrease in responsive B cells, leading to increased susceptibility to viral and bacterial infection
A decrease in immunosurveillance activity, leading to higher rates of cancer

3
 Involution of the thymus, leading to fewer T cells in circulation

AIDS
an immunodeficiency diseaseAIDS is an immunodeficiency disease that results from a viral
infection that targets helper T cells. We discuss AIDS in the Clinical Note on the next page.

Which disorder involves a virus binding to CD4 proteins, and the subsequent infection
of helper T cells? acquired immune deficiency syndrome (AIDS)
(Acquired Immunodeficiency Syndrome) is a condition in which a person experiences an
assortment of infections caused by progressive destruction of immune system cells. It is
the end stage of infection of a person by human immunodeficiency virus (HIV).

• 36 million people were living with HIV worldwide at the end of 2012 (WHO est).

• HIV is present in the blood and some body fluids, transmission occurs through exchange of bodily
fluids.
- Unprotected sex, contaminated needles, transmission between mother and baby during birth or
breast-feeding

• HIV does not survive long outside the body, so it cannot be transmitted by casual physical contact
with an infected person such as hugging

• HIV is a retrovirus, meaning its genetic info is carried as RNA (not DNA). It is unable to replicate
on it's own, but used the infected host cell's machinery to make copies of itself, which then leave the
cell (which ruptures and dies) and go on to infect other cells.

• HIV mainly damages T cells. Over time, the bodies ability to replace T cells is slowly diminished.

AIDS: Signs & Symptoms

• Soon after infection (3 wks to 3 months) w HIV brief flu-like illness occurs (fever, fatigue, headache,
joint pain, etc)

• As early as 3-4 weeks post-HIV infection plasma antibodies begin to accumulate (HIV positive means
someone tests positive for anti-HIV plasma antibodies)

• Over time (2-10 years) as T cells diminish immunodeficiency symptoms occur: enlarged lymph nodes,
persistent fatigue, weight loss, night sweats, rashes, diarrhea, lesions of the mouth and gums

• Eventually diminished immune system leaves the infected individual susceptible to opportunistic
infections, which are typically the cause of death.
- Opportunistic infections involve organisms that do not usually cause disease but do so when the immune
system is depressed (pneumocystis pneumonia, tuberculosis, etc)

• AIDS = helper T cell count below 200 (down from ~1200) cells per microliter of blood or when
opportunistic infections arise (whichever occurs first)

AIDS: Treatment
Infection with HIV cannot be cured. Drugs that extend the life of HIV-infected individuals include:

• Reverse transcriptase inhibitors: Block RNA --> DNA

• Protease inhibitors: Block the assembly of new viruses
• HAART: Highly active antiviral therapy is a combo of RT inhibitors + protease inhibitors. Works well

4
 (delays progression and even eliminates opportunistic infections) but is costly and has extremely toxic side
effects for some.
• (Still working on integrase inhibitors for blocking the insertion of viral DNA --> host DNA)
• Viral load test has been developed that measures the number of viral RNA molecules in a mL of blood, a
good predictor of how soon an HIV infected person will develop AIDS. Also detects developing resistance
to a drug.
• Long-term goal: develop an HIV vaccine to prevent infection

Allergic Reactions
Allergic reactions involve IgE antibodies. IgE antibodies cause mast cells and basophils to release
histamine and lead to an inflammatory response
• Constricted airways, runny nose from excess mucus secretion

Life-threatening allergic reactions result in anaphylaxis (insect bites/stings, meds, foods)

• Massive release of histamine from mast cells causes rapid response that involves hypotensive shock
as vasodilation occurs à BP drops
• Treated with epinephrine
Allergic
Allergic (hypersensitive): Overly reactive to a substance that is tolerated by most people.
Histamines, leukotrienes, and other chemicals that cause pain and inflammation are
released when mast cells and basophils are stimulated in an allergic reaction

Allergen
Antigens that induce an allergic reaction

allergic rhinitis
(inflammed nasal membranes) includes hay fever.

Anaphylaxis
is an immune response to a circulating antigen that stimulates mast cells throughout the body to
release chemicals that prompt the inflammatory response.anaphylaxic shock
In anaphylaxis, a circulating allergen affects MAST cells throughout the body
mast
Anaphylactic shock.
An allergen circulating in the bloodstream affects mast cells throughout the body, dropping blood
pressure to dangerously low levels.

Antibody
antigen-specific protein secreted by plasma cells; immunoglobulin
antibodies—substances that recognize the antigens on foreign microbes and act as tags that identify
the invaders.
Antibody Action
1. Neutralizing antigen = neutralizes some bacterial toxins and prevents attachment of some

viruses to body cells

2. Immobilizing bacteria = if antibody against antigens on cilia or flagella of motile bacteria,

may cause bacteria to lose motility, limiting spread

3. Agglutinating and precipitating antigen = b/c antibodies have more than one binding site for

5
 antigens, they may cross-link pathogens to each other causing agglutination (clumping together).

Phagocytic cells ingest agglutinated microbes more readily.

4. Activating complement = antigen-antibody complexes initiate complement system

5. Enhancing phagocytosis = Stem region of antibody acts as flag that attracts more phagocytes

once antigen bound to antibody's variable region. The antibodies also coat the microbes so more

susceptible to phagocytosis.

elminate antigens by

1. creating an immune complex that can lead to precipitation

2. by making viruses and toxins incapable of attaching to a cell through
neutralization
3. by activating the complement system

Antibody Molecule structure

An antibody molecule consists of two parallel pairs of polypeptide chains: one pair of heavy chains
and one pair of light chains. Each chain contains both constant segments and variable segments.

• Consists of two parallel polypeptide chains

• One pair of heavy chains
• One pair of light chains
• Each pair contains:
• Constant segments
• On heavy chains, form the base of antibody molecule
• Variable segments
• Free tips are antigen binding sites
• Differences in amino acid sequences produce variability needed for different
antibodies
• A Y-shaped antibody molecule consists of two pairs of polypeptide chains: one pair
of heavy chains and one pair of light chains Each chain contains both constant
segments and variable segments.
• The constant segments of the heavy chains form the base of the antibody molecule
(see Figure 22–24a,b). B cells produce only five types of constant segments. These are
the basis of a scheme that identifies five classes of antibodies, or immunoglobulins
(Igs): IgG, IgE, IgD, IgM, and IgA (Table 22–1). The structure of the constant segments
of the heavy chains determines the way the antibody is secreted and how it is distributed
within the body. For example, antibodies in one class circulate in body fluids, whereas
those of another class bind to the membranes of basophils and mast cells.
• The heavy-chain constant segments, which are bound to constant segments of the light
chains, also contain binding sites that can activate the complement system. These binding
sites are covered when the antibody is secreted but become exposed when the antibody
binds to an antigen.

6
 • The specificity of an antibody molecule depends on the amino acid sequence of the
variable segments of the light and heavy chains. The free tips of the two variable
segments form the antigen-binding sites of the antibody molecule (see Figure 22–24a).
The heavy-chain constant segments have no effect on the antibody’s specificity, which is
determined by the antigen-binding sites.

Antibody-mediated immunity (HUMORAL)

-most effective in viral and bacterial infections

B cells release antibodies from within lymphatic organs/tissues which circulate through the
lymph/blood to reach the site of invasion and disable the antigen

1) B CELLS ARE ACTIVATED BY A SPECIFIC ANTIGEN

Antigen binds to unique receptors on specific B cells
B cells endocytize and process antigen, and display it

2) HELPER T CELLS COSTIMULATE THE B CELL

Bind to the antigen displayed by the B cell
Costimulate the B cell via surface molecules and cytokines

3) B CELLS UNDERGO CLONAL SELECTION

Produce plasma cells (effector cells) that produce antibodies to the antigen
Produce memory B cells that can quickly differentiate into more plasma and memory B cells in the
event of a future encounter with the antigen

4) ANTIBODIES DISABLE THE ANTIGEN, MEMORY CELLS WAIT

In antibody-mediated (humoral) immunity, B cells secrete antibodies that defend against
antigens and pathogens in body fluids.
Without helper T cells—which promote B cell division, the maturation of plasma cells, and antibody
production by plasma cells—the antibody-mediated immune response would probably not occur.

antigen–antibody complex
When an antigen-binding site on an antibody molecule binds to its corresponding antigen
molecule, an antigen–antibody complex is formed. Once the two molecules are in
position, hydrogen bonding and other weak chemical forces lock them together. Antigen-
binding sites interact with an antigen in the same way that the active site of an enzyme
interacts with a substrate molecule
antigen
molecule recognized by the receptors of B and T lymphocytes

antigen presentation
Antigen presentation occurs when an antigen–glycoprotein combination appears in the plasma
membrane of an antigen-presenting cell (typically of a macrophage or dendritic cell). T cells
sensitive to this combination are activated if they contact the membrane of the antigen-presenting
cell.

the presence of antigens or antigenic fragments on plasma membranes

binding of processed antigen to the protein-binding cleft of a major histocompatibility complex
molecule. Antigen presentation occurs when an antigen-glycoprotein, or antigen-MHC

7
 protein, combination capable of activating T cells appears in a plasma membrane. T cells
sensitive to this antigen are activated if they contact the antigen on the plasma membrane
of the antigen-presenting cell.
Antigen presentation may stimulate both cell-mediated immunity and antibody-mediated
immunity.

steps Antigen presentation occurs when an antigen-glycoprotein complex capable of

activating T cells appears in a plasma membrane. Place the steps in the correct order to
outline how most body cells find and present antigens.

1. Body cells becomes infected by virus or bacterium

2 Abnormal peptides appear in the cytoplasm.
3. The endoplasmic reticulum incorporates abnormal peptides as it synthesizes Class I
MHC.
4. The Golgi apparatus packages Class I MHC into secretory vesicles
5. Class I MHC displays abnormal peptides on the plasma membrane.

Antigen processing
internalization and digestion of antigen in an antigen-presenting cell
Antigen Processing
• APC encounters antigen
• Internalizes it by endocytosis
• Digests it into molecular fragments
• Displays relevant fragments (epitopes) in the grooves of the MHC protein
• Before an antigen can stimulate a lymphocyte, it must first be processed
by an anitgen presenting cell such as macrophage. Macrophages
specialize in phagocytosing pathogens and digesting components from
their structures, such as pieces of cell wall. After the digestion, this piece
of material becomes a “tag,” or antigen, that is bound to the
macrophage’s surface. This antigen presented by the macrophage is like
blood presented to a bloodhound and is then used as a homing signal by
which to target pathogens.
antigen elemination:
1. Neutralization
• Antibodies occupy binding sites on viruses and bacterial toxins preventing them from
affecting body cells

8
 2. Prevention of pathogen adhesion
• IgA antibodies in glandular secretions cover bacteria or viruses preventing penetration of
body surfaces
3. Activation of complement
• After antigen binding, complement also can bind to the antibody, accelerating the
complement cascade
4. Stimulation of inflammation
• Basophil and mast cell stimulation to release chemicals
5. Opsonization
• Coating of pathogen with antibodies allows phagocytes to bind easier
6. Attraction of phagocytes
• Attached antibodies attract eosinophils, neutrophils, and macrophages
7. Precipitation and agglutination
• Antibodies can bind to antigenic determinant sites on adjacent antigens
• The linking of multiple pathogens by antibodies creates an immune complex
• Formation of insoluble complexes (too large to stay in solution) is called
precipitation
• Formation of an immune complex from surface antigens is called agglutination
• Example: clumping of RBCs in a transfusion reaction

antigen receptor
two-chain receptor by which lymphocytes recognize antigen

antigenic determinant
(also, epitope) one of the chemical groups recognized by a single type of lymphocyte antigen
receptor

Artificially acquired active immunity

develops after receiving a vaccine.
(APCs)
antigen presenting cells
the process the antigen to activate t cells and secrete substance to dvide t cells and b cells
Antigen-presenting cells are differentiated from other body cells by the presence of Class
II MHC proteins in their plasma membranes. Which of the following correctly describes a
difference between Class I and Class II MHC?
Macrophages use Class II MHC to display antigens they have phagocytized.

AUTOantibodys
When the recognition system does not work correctly, however, activated B cells make
antibodies against other body cells and tissues. These “misguided” antibodies are
called autoantibodies. The trigger may be a reduction in suppressor T cell activity, the excessive
stimulation of helper T cells, tissue damage that releases large quantities of antigenic fragments,
haptens bound to compounds normally ignored, viral or bacterial toxins, or a combination of
factors.

The resulting condition depends on the antigen that the autoantibodies attack. For example:

 The inflammation of thyroiditis is due to autoantibodies against thyroglobulin.

 Rheumatoid arthritis occurs when autoantibodies form immune complexes in connective
tissues around the joints.

9
  Type 1 diabetes develops when autoantibodies attack cells in the pancreatic islets

Autoimmune disorders
• Malfunction of the body’s self recognition system
• Activated B cells make antibodies against “self” antigens or body cells and tissues (Called
autoantibodies)
• May result from similarity of foreign antigen to body cells
• Example: protein in measles virus contains amino acid sequences similar to those of
myelin proteins, so antibodies targeting the viruses may also target myelin sheaths
(likely mechanism for multiple sclerosis)
• Risk increases if a person has an unusual type of MHC protein
• Examples of autoimmune disorders
• Thyroiditis (inflammation resulting from autoantibodies attacking
thyroglobulin)
• Rheumatoid arthritis (autoantibodies attack connective tissues around
joints)
• Type 1 diabetes mellitus (autoantibodies attack pancreatic islet cells)
• Multiple sclerosis (autoantibodies attack myelin)
Axillary nodes
-drain the legs

B
B cells
How is a sensitized B cell activated?
Contact with a helper T cell
A sensitized B cell comes in contact with a helper T cell that has already been activated by antigen
presentation by the same antigen that caused B cell sensitization. The helper T cell binds to the B cell’s
MHC complex, recognizes the antigen, and begins secreting cytokines, which promote B cell activation.
After activation of the B cell, these same cytokines stimulate B cell division, speed up plasma cell
formation, and enhance antibody production.

• mature into plasma cells

• Produce antibodies that inactivate pathogens
• Involved in antibody-mediated immunity (fights extracellular pathogens- viruses, bacteria,
fungi in body fluids outside cells)
o B cells
 Mature and move into lymph nodes, spleen, and other lymphoid tissue

lymphocytes that act by differentiating into an antibody-secreting plasma cell

• Antibody-mediated defenses (B cells)
B cell sensitization and activation
• Sensitization: Preparation for activation
• Antigens are brought into cell through endocytosis and then placed on
surface of cell bound to Class II MHC proteins
• Full activation requires helper T cell
• Helper T cell must have been activated by exposure to the same
antigen
• Helper T cell binds to MHC complex of sensitized B cell
• Secretes cytokines to promote B cell activation
• B cell activation
• B cells go through series of divisions to produce two types of daughter cells

10
 • Memory B cells
• Inactive until 2nd exposure to antigen
• Respond then by differentiating into plasma cells
• Plasma cells
• Activated B cells, each capable of secreting up to 100
million antibody molecules per hour
•
Upon subsequent exposure to injuries or infections that induce the same antigen, memory B cells
respond by differentiating into plasma cells.
•
B lymphocytes differentiate into memory and plasma cells. During the stimulation of an adaptive
immune response, a specific antigen activates one clonal lineage of B lymphocyte, which in turn
differentiates into memory and plasma cells. The plasma cells produce specific antibodies to the
antigen during the response. This production may take several weeks if this is the first time the antigen
has been detected in the body. Memory cells survive for years after the initial response and enable the
body to react quickly if this antigen is encountered again.

A B cell is sensitized by exposure to antigens. Once antigens are bound to antibodies in the B cell plasma
membrane, the B cell displays those antigens on class II MHC proteins in its plasma membrane. Activated
helper T cells encountering the antigens release cytokines that costimulate the sensitized B cell and trigger its
activation. The activated B cell then divides, producing memory B cells and plasma cells that secrete
antibodies
Recall that B cell plasma membranes contain class II MHC proteins. During sensitization,
antigens are brought into the cell by endocytosis. The antigens subsequently appear on the
surface of the B cell, bound to class II MHC proteins. The sensitized B cell is then on “standby”
but generally does not undergo activation unless it receives the “OK” from a helper T cell. The
need for activation by a helper T cell helps prevent inappropriate activation, the same way that
costimulation acts as a “safety” in cell-mediated immunity.

What happens when a sensitized B cell meets a helper T cell that has already been activated by
antigen presentation? The helper T cell binds to the B cell’s MHC complex, recognizes the
antigen, and begins secreting cytokines that promote B cell activation

bacterial infection :
activation of B cells
activation of cytotoxic T cells
phagocytosis by macrophages and APCs
NO release of interferon

barrier defenses
antipathogen defenses deriving from a barrier that physically prevents pathogens from entering the
body to establish an infection

blood thymus barrier

It is found in the cortex of the thymus.

11
 epithelial reticular cells (ERCs). Epithelial reticular cells regulate T cell develop-ment and function.
ERC processes also encircle the capillaries in the cortex and maintain the blood thymus barrier

bone marrow
tissue found inside bones; the site of all blood cell differentiation and maturation of B lymphocytes

bronchus-associated lymphoid tissue (BALT)

lymphoid nodule associated with the respiratory tract

C
cancer
The increased incidence of cancer in elderly people may result from a decline in immune
surveillance, which results in reduced elimination of tumor cells as they arise.

capsule
is dense connective tissue

capillary
Lymphatic capillaries are lined by endothelial cells, but the basement membrane is incomplete or
absent. the endothelial cells overlap acting as one-way valves

CD markers
CD markers refer to a class of membrane proteins. CD is an abbreviation for “cluster of
differentiation.” T cell plasma membranes contain CD proteins. T cells with CD8
markers respond to antigens presented by class I MHC proteins. T cells with CD4
markers respond to antigens presented by class II MHC proteins.
• Class of proteins containing membrane proteins involved in antigen recognition
• CD stands for “cluster of differentiation”
• Two classes associated with T cell
1. CD8 markers (on CD8 T cells) CD8 markers are found on cytotoxic T cells,
memory TC cells, and regulatory T cells
• Respond to Class I MHC proteins
2. CD4 markers (on CD4 T cells) CD4 markers are on all helper T cells
• Respond to Class II MHC proteins
II VS I
Macrophages use Class II MHC to display antigens they have phagocytized.
Cells present antigens on Class I MHC if the antigen has infected them. Antigen-presenting cells actively
seek out pathogens in the tissues, phagocytize all or part of them, and digest them in lysosomes. The
remaining fragments are displayed on Class II MHC.

CD4 T cells: Respond to Class II MHC proteins

respond to antigens presented by Class II MHC proteins.
Before they can initiate antibody-mediated immunity, inactive CD4 T cells must be exposed to
appropriate antigens bound to Class II MHC proteins.A CD4 T cell can recognize antigens bound to
Class I MHC proteins.

CD8 T cell types Respond to Class I MHC proteins

12
 1. Cytotoxic T cells (TC cells)
• Seek out and destroy abnormal and infected cells in injured tissues
• Target cells must have specific Class I MHC proteins
• Destructive mechanisms
• Release of perforins
• Activate target cell self-destruction genes for cell death (apoptosis)
• Disruption of cell metabolism with lymphotoxin
2. Memory TC cells
• Produced but do not differentiate further during first antigen exposure
• Upon 2nd exposure to same antigen, memory TC cells become cytotoxic T cells
3. Suppressor T cells
• Secrete suppression factors to limit responses of other T cells and B cells
• Also act only after first antigen exposure (initial immune response)
2.
The primary response of CD8 T cell differentiation in cell-mediated immunity is the
production of cytotoxic T cells. This subtype of T lymphocytes is responsible for the
classic cell-mediated immune response. This type of response involves a direct physical
attack by highly mobile cytotoxic T cells, which have the ability to infiltrate peripheral
tissues and destroy abnormal as well as infected cells, such as those exposed to viruses.
Cytotoxic T cells can kill target cells by way of perforin to cause cell lysis or through the
secretion of lymphotoxin. These T cells may also cause target cells to undergo
programmed cell death.
3. The active cytotoxic T cells destroy the infected body cells or abnormal
cells using several mechanisms. They secrete perforin to destroy the
cell’s membrane, cytokines to stimulate apoptosis or programmed cell
death, and lymphotoxin to disrupt the cell’s metabolism.
Cell-mediated immunity (cellular immunity)
In cell-mediated (cellular) immunity, T cells defend against abnormal cells and pathogens
inside cells
Cytotoxic T cells directly attack target cells containing intracellular pathogens, some cancer cells, and
tissue transplants

1) T CELLS ARE ACTIVATED BY A SPECIFIC ANTIGEN

• Antigen binds to specific T cell rc on unique cells displaying it
• Costimulation occurs: T cell receives a 2nd signal (such as IL-2)

2) ACTIVATED T CELLS UNDERGO CLONAL SELECTION

• Divide and differentiate to form a clone of cytotoxic T cells (identical population that all recognize
the same antigen)
• Includes effector (active) and memory cytotoxic T cells

3) EFFECTOR T CELLS CARRY OUT IMMUNE RESPONSES THAT ELIMINATE THE

INTRUDER
• Recognize and attach to target cells
• Trigger apoptosis in (granzymes/fragmentins) and create channels in (perforins) the membrane of the
infected cells, also create channels in the microbes cell membrane
• Attract and activate phagocytes to the area

4) MEMORY T CELLS DO NOT ACTIVELY PARTICIPATE IN THE INITIAL IMMUNE

RESPONSE

13
 • Respond to antigen in the future by swiftly proliferating and differentiating into more effector and
memory T cells to combat it
In cell-mediated (cellular) immunity, T cells defend against abnormal cells and pathogens inside
cells. In antibody-mediated (humoral) immunity, B cells secrete antibodies that defend against
antigens and pathogens in body fluids.

Central Tolerance
B cell tolerance induced in immature B cells of the bone marrow
central arteries Finer branches of trabecular arteries, which are surrounded by
areas of white pulp

chemokine
soluble, long-range, cell-to-cell communication molecule

chronic inflammation
inflammation occurring for long periods of time

chyle
lipid-rich lymph inside the lymphatic capillaries of the small intestine

cisterna chyli
saclike chamber that receives lymph from the inferior part of the abdomen, the pelvis, and the
lower limbs
forms the beginning of the thoracic duct
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the
lower limbs by way of the right and left lumbar trunks and the intestinal trunk
• Expanded, saclike chamber at the base of the thoracic duct
• Receives lymph from:
• The inferior part of the abdomen
• The pelvis
• The lower limbs
• Lymph is drained into the cysterna chyli by the:
• Lumbar trunks
• Intestinal trunk

right lymphatic duct collects lymph from the right side of the body superior to the diaphragm
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the lower
limbs by way of the right and left lumbar trunks and the intestinal trunk
The right lymphatic duct is formed by the merging of the right jugular, right subclavian,
and right bronchomediastinal trunks in the area near the right clavicle. This duct empties into
the right subclavian vein, delivering lymph from the right side of the body superior to the
diaphragm

Class I MHC proteins

The three major types of T cells activated by class I MHC proteins are cytotoxic T cells,
memory TC cells, and regulatory T cells.

14
 class switching
ability of B cells to change the class of antibody they produce without altering the specificity for
antigen
Class I MHC proteins are in all nucleated body cells.

CD8 T cell types Respond to Class I MHC proteins

class II MHC proteins are only in antigen-presenting cells (APCs) and lymphocytes.

1. Cytotoxic T cells (TC cells)

• Seek out and destroy abnormal and infected cells in injured tissues
• Target cells must have specific Class I MHC proteins
• Destructive mechanisms
• Release of perforins
• Activate target cell self-destruction genes for cell death (apoptosis)
• Disruption of cell metabolism with lymphotoxin
2. Memory TC cells
• Produced but do not differentiate further during first antigen exposure
• Upon 2nd exposure to same antigen, memory TC cells become cytotoxic T cells
3. Suppressor T cells
• Secrete suppression factors to limit responses of other T cells and B cells
• Also act only after first antigen exposure (initial immune response)
4. II VS I
5. Macrophages use Class II MHC to display antigens they have phagocytized.
6. Cells present antigens on Class I MHC if the antigen has infected them. Antigen-presenting cells
actively seek out pathogens in the tissues, phagocytize all or part of them, and digest them in
lysosomes. The remaining fragments are displayed on Class II MHC.
7.
8. CD4 T cells: Respond to Class II MHC proteins
9. respond to antigens presented by Class II MHC proteins.
10. Before they can initiate antibody-mediated immunity, inactive CD4 T cells must be exposed to
appropriate antigens bound to Class II MHC proteins.A CD4 T cell can recognize antigens bound to
Class I MHC proteins.
All T cells have a CD3 receptor complex in their plasma membranes, and this complex ultimately activates the T cell. Either of two
other CD markers may be bound to the CD3 receptor complex, and these two CD markers are especially important in specific groups
of T cells:
 CD8 markers are found on cytotoxic T cells and regulatory T cells, which together are often called CD8 T cells. CD8 T cells
respond to antigens presented by class I MHC proteins.
 CD4 markers are found on helper T cells, often called CD4 T cells. CD4 T cells respond to antigens presented by class II MHC
proteins.

T cells are not usually activated upon their first encounter with the antigen. Antigen recognition simply prepares the cell for activation.

clonal anergy
process whereby B cells that react to soluble antigens in bone marrow are made nonfunctional

clonal deletion
removal of self-reactive B cells by inducing apoptosis

15
clonal expansion
growth of a clone of selected lymphocytes

clonal selection
-stimulating growth of lymphocytes that have specific receptors
-The process by which a lymphocytes divides and differentiates in response to contact with a specific
antigen

clone
group of lymphocytes sharing the same antigen receptor
Regarding adaptive immunity, what is meant by a clone of cells?

A population of cells sensitive to a specific antigen

Thousands of lymphocytes are not enough to overcome a pathogenic invasion. However, when
activated by a specific antigen, a lymphocyte begins to divide, producing more lymphocytes with the
same specificity. All the cells produced by these divisions make up a clone, of which all members are
sensitive to the same specific antigen. The process of an antigen selecting a particular lymphocyte for
cloning is call clonal expansion

complement
enzymatic cascade of constitutive blood proteins that have antipathogen effects, including the direct
killing of bacteria
Complement proteins are a group of over 30 circulating proteins which function as part of the innate,
non-specific immune response. When activated, these proteins will stimulate inflammation during
tissue injury.
Complement activation also results in the attraction of phagocytes.
Complement activation will also cause destruction of target cell membranes and will result in lysis of
pathogens.
complement activation can happen from 1 of 3 pathways:
1)  The classical pathway activates the complement system most rapidly and
effectively. Its proteins are abbreviated “C” with a number that corresponds to its
discovery. It begins with the binding of complement protein C1 to two nearby
antibodies already attached to its specific antigen, such as a bacterial cell wall.
2)  The lectin pathway activates the complement system by the binding of the
protein mannose-binding lectin (MBL) to carbohydrates on pathogen surfaces,
such as bacterial cell walls.
3) The alternative pathway also activates the complement system without antibody
interactions. Its proteins are given specific names or called factors. The
alternative pathway begins when several complement proteins—
including properdin (factor P), factor B, and factor D—interact in the plasma.
This interaction is triggered by exposure to foreign materials, such as the cell wall
of a bacterium.

complement activation 
Inflammation
Attraction of phagocytes and enhancement of phagocytosis
Destruction of target cell membranes
NOT fever

16
Complement System
-Defensive system made up of 30+ proteins produced by the liver and found circulating in blood

plasma and within tissues throughout the body

-These proteins destroy microbes by causing phagocytosis, cytolysis, inflammation

-They also prevent excessive damage to body tissues

-Named C1-C9 in order that were discovered

-They are inactive until become activated when split by enzymes into active fragments,

designated by a and b

-Some complement proteins called factors B, D, P (properdin)

-Act as a cascade = one reaction triggers another etc.

-Complement activation can begin in one of three ways, all of which activate C3, after which

cascade begins that causes phagocytosis, cytolysis, and inflammation.

Complement Cascade

1. Inactivated C3 splits into activated C3a and C3b

2. C3b binds to surface of a microbe and receptors on phagocytes attach to C3b (i.e.

enhances phagocytosis by coating microbe, a process called opsonization, which

promotes attachment of phagocyte to microbe)

3. C3b also initiates series of reactions that cause cytolysis (C3b splits C5; C5b fragemnt

binds to C6 and C7, which attach to plasma membrane of invading microbe; C8 and

several C9 molecules join other complement proteins and form a cylinder-

shaped membrane attack complex, which inserts into plasma membrane)

4. MAC attack complex creates channels in plasma membrane that results in cytolysis

5. C3a and C5a bind to mast cells and cause them to release histamine that increases

17
 blood vessel permeability during inflammation. C5a also attracts phagocytes to site of

inflammation (chemotaxis)

Activation of C3
1. Classical pathway - when antibodies bind to antigens. Antigen-antibody complex

binds and activates C1, which leads to C3

2. Alternative Pathway - does not involve antibodies; involves interaction between

lipid-carbohydrate complex on sfc. of microbes and factors B, D, P, activates C3

3. In Lectin pathway, macrophages that digest microbes release chemicals that cause

liver to produce proteins called lectins. Lectins bind to carbs on sfc. of microbes, leading

to activation of C3.

What happens to C3 once it is activated?

After it activates the complement, proteins in blood and body cells (e.g. blood cells)
break down activated C3 to cease destructive capabilities quickly, minimize damage to
body cells.

constant region domain

part of a lymphocyte antigen receptor that does not vary much between different receptor types

costimulation
secondary binding process, essentially confirms the initial activation signal.
It helps prevent T cells from mistakenly attacking normal (self) tissues. If a cell displays
an unusual antigen but does not display the “I am an active phagocyte” or “I am infected”
signal, T cell activation will not occur. Costimulation is important only in determining
whether a T cell will become activated.

Once activation has occurred, the “safety” is off and the T cell will undergo mitosis,
producing clones of identical cells. The types of cells that are produced depend on the
type of T cell that was activated

cortex
Deep cortex (paracortex)- Dominated by T cells

Outer cortex- Contains B cells within germinal centers that resemble those of lymphoid nodules

18
cytokine
soluble, short-range, cell-to-cell communication molecule
chemicals that tissue cells release to coordinate local activities. Cytokines include hormones and paracrine-like glycoproteins
important to the immune response. Most cells produce cytokines only for paracrine communication—that is, cell-to-cell
communication within one tissue

cytotoxic T cells (Tc)

The active cytotoxic T cells destroy the infected body cells or abnormal cells using several
mechanisms.
1. They secrete perforin to destroy the cell’s membrane,
2. cytokines to stimulate apoptosis or programmed cell death,
3. and lymphotoxin to disrupt the cell’s metabolism.

The primary response of CD8 T cell differentiation in cell-mediated immunity is the production of  cytotoxic T cells. 
CYTOTOXIC T CELLS
• Directly kill infected body cells
• Involved in cell-mediated immunity (fights intracellular pathogens, cancer cells, foreign tissue
transplants)
Cytotoxic T cells and NK cells can be activated by direct contact with virus-infected cells.
A cytotoxic T cell (TC cell) destroys its target cell by first encountering its target antigen bound to a
class I MHC protein. It then attacks it by any one of the following mechanisms: (1) destroying the
target cell’s membrane through the release of PERFORINS; (2) activating apoptosis in the target cell;
(3) disrupting the target cell’s metabolism through the release of lymphotoxin

Cytotoxic T cells are the T cells responsible for seeking out and destroying abnormal or infected cells.
Cytotoxic T cells are the part of the adaptive immune system that launches a direct attack on
pathogens. These direct attacks usually end with the target cells being lysed. Most cytotoxic T cells
contain perforins and other compounds that cause direct damage to the cell membranes of pathogens,
which results in their destruction.
1. Cytotoxic T cells (AKA Killer T-cells)
• Attack foreign cells or body cells infected by viruses
• Attack commonly involves direct contact
• Primary cells involved in production of cell-mediated immunity (cellular immunity)
2. The T cell may (1) release perforins to destroy the target cell’s plasma membrane, (2)
release cytokines and activate genes in the target cell’s nucleus telling that cell to undergo
apoptosis, or (3) secrete a poisonous lymphotoxin (lim-fō-TOK-sin) to kill the target
cell.
DECREASE in the number of cytotoxic T cells would affect which type of immunity? 
Answer: A decrease in the number of cytotoxic T cells would affect cell-mediated immunity,
reducing the effectiveness of cytotoxic T cells in killing foreign cells and virus-infected cells.

The primary response of CD8 T cell differentiation in cell-mediated immunity is the production
of cytotoxic T cells. This subtype of T lymphocytes is responsible for the classic cell-mediated
immune response. This type of response involves a direct physical attack by highly mobile cytotoxic T
cells, which have the ability to infiltrate peripheral tissues and destroy abnormal as well as infected
cells, such as those exposed to viruses. Cytotoxic T cells can kill target cells by way of perforin to cause
cell lysis or through the secretion of lymphotoxin. These T cells may also cause target cells to undergo
programmed cell death.

D
delayed hypersensitivity

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 (type IV) T cell-mediated immune response against pathogens infiltrating interstitial tissues, causing
cellular infiltrate

dendritic cells or macrophages

cells present the antigen to the lymphocytes, thus activating the lymphocytes located in the lymphoid
follicles

diapedesis-
Phagocytes can leave capillaries by squeezing between adjacent endothelial cells.

ducts
right lympatic duct empties lymph into right subclavian vein

thoratic duct drains into left brachiocephalic vein

right lymphatic duct collects lymph from the right side of the body superior to the diaphragm
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the lower
limbs by way of the right and left lumbar trunks and the intestinal trunk
The right lymphatic duct is formed by the merging of the right jugular, right subclavian,
and right bronchomediastinal trunks in the area near the right clavicle. This duct empties into
the right subclavian vein, delivering lymph from the right side of the body superior to the
diaphragm

E
early induced immune response
includes antimicrobial proteins stimulated during the first several days of an infection

Effector cells
Carry out immune responses that ultimately destroy or inactivate the antigen

efferent lymphatic vessels

lead out of a lymph node

Elephantiasis
• AKA-Lymphatic filariasis
• Caused by blocked/obstruction of lymphatic drainage
• Lymphatic filariasis is a parasitic disease caused by microscopic, thread-like worms that
only live in the human lymph system.
• Elephantiasis is when the skin and underlying tissues become abnormally thick. This is
often the result of secondary bacterial infections that happen because the body's immune
system is damaged due to the parasite.
Eosinophils-
Less abundant; phagocytize foreign compounds or pathogens that have been coated with antibodies
-are cells that phagocytize foreign compounds or pathogens that have been coated with antibodies.
These are among the cells that provide the “first line of cellular defense” against pathogenic invasion.
phagocyte

20
Epitopes
Small parts of large antigen molecules that trigger immune responses
Antibodies do not bind to the entire antigen. Instead, they bind to specific portions of its exposed
surface—regions called antigenic determinant sites, or epitopes (Figure 22–24c). The
specificity of the binding depends initially on the three-dimensional “fit” between the variable
segments of the antibody molecule and the corresponding antigenic determinant sites.
A complete antigen has at least two antigenic determinant sites, one for each of the antigen-
binding sites on an antibody molecule. Exposure to a complete antigen can lead to B cell
sensitization and a subsequent immune response. Most environmental antigens have multiple
antigenic determinant sites, and entire microorganisms may have thousands.

erythroblastosis fetalis
disease of Rh factor-positive newborns in Rh-negative mothers with multiple Rh-positive children;
resulting from the action of maternal antibodies against fetal blood

F
fas ligand
molecule expressed on cytotoxic T cells and NK cells that binds to the fas molecule on a target cell
and induces it do undergo apoptosis

Fc region
in an antibody molecule, the site where the two termini of the heavy chains come together; many
cells have receptors for this portion of the antibody, adding functionality to these molecules

Fever-
Accelerate(s) tissue metabolism and the activity of defenses (innate)
Pyrogens increase body temperature (produce a fever), which can mobilize defenses,
accelerate repairs, and inhibit pathogens.
The high body temperatures of a fever may inhibit some viruses and bacteria or increase
their reproductive rate so that the disease runs its course more quickly. High body
temperatures also accelerate the body’s metabolic processes, which may help to mobilize
tissue defenses and speed the repair process.
• high levels of Pyrogens indicate fever
Fever
• Body temperature >37.2°C (99°F)
• Pyrogens
• Circulating fever-inducing proteins
• Reset temperature thermostat in hypothalamus
• Raises body temperature
• Can be beneficial within limits
• May inhibit some viruses and bacteria
• Increases metabolic rate which may accelerate tissue defenses and repair
process
• Within limits, a fever can be beneficial. High body temperatures may inhibit some
viruses and bacteria. The most likely benefit is on body metabolism. For each 1 °C rise in
body temperature, metabolic rate increases by 10 percent. Cells can move faster, and

21
 enzymatic reactions take place more quickly. As a result, tissue defenses can be
mobilized more rapidly and the repair process speeds up.
 Fibroblasts
then begin forming scar tissue that reinforces the clot and slows the invasion of adjacent
tissues (stimulated by  cytokines released by active phagocyte)

Fixed macrophage
Microglia
Stellate macrophages
Histiocytes
Fixed macrophages, or histiocytes, reside in specific tissues and organs. These cells
are normally incapable of movement, so their targets must diffuse or otherwise move
through the surrounding tissue until they are within range. Fixed macrophages are
scattered among connective tissues, usually in close association with collagen or reticular
fibers. They are found in the papillary and reticular layers of the dermis, in the
subarachnoid space of the meninges, and in bone marrow. In some organs, the fixed
macrophages have special names. Microglia are macrophages in the central nervous
system, and stellate macrophages (Kupffer cells) are macrophages located on the
luminal surface of liver sinusoids.
Free macrophages, or wandering macrophages, travel throughout the body. They
arrive at the site of an injury by migrating through adjacent tissues or by leaving the
circulating blood. Some tissues contain free macrophages. For example, alveolar
macrophages, also known as dust cells, monitor the epithelial surfaces of the lungs for
respiratory pathogens.
• Free macrophages and microphages function in similar ways:
• Both can move through capillary walls by squeezing between adjacent endothelial cells. This process is known as emigration. 
The endothelial cells in an injured area develop membrane “markers” that signal passing blood cells that something is wrong. The
phagocytes then attach to the endothelial lining and migrate into the surrounding tissues.
• Both may be attracted to or repelled by chemicals in the surrounding fluids, a phenomenon called chemotaxis. They are particularly
sensitive to chemicals known as cytokines that are released by other body cells and to chemicals released by pathogens.
• For both, phagocytosis begins with adhesion, the attachment of the phagocyte to its target. In adhesion, receptors on the plasma
membrane of the phagocyte bind to the surface of the target. Adhesion is followed by the formation of a vesicle containing the bound
target The contents of the vesicle are digested once the vesicle fuses with lysosomes or peroxisomes.

G
gastrosplenic ligament,
broad band of mesentery. The spleen is attached to the lateral border of the stomach by the
gastrosplenic ligament

germinal centers
clusters of rapidly proliferating B cells found in secondary lymphoid tissues

graft-versus-host disease
in bone marrow transplants; occurs when the transplanted cells mount an immune response against
the recipient

granzyme

22
 apoptosis-inducing substance contained in granules of NK cells and cytotoxic T cells

H
haptens
incomplete antigen
do not ordinarily cause b cells tpo activate can attach to carrier molecules forming combo that can act
as complete antigen
Haptens include short peptide chains, steroids and other lipids, and several drugs, including
antibiotics such as penicillin

helper T cells (Th)

Helper T cells “help” translate the message from the antigen-presenting cells of the
nonspecific response to the cells of the specific immune responses.

helper T cells play a crucial role in antibody-mediated immunity by stimulating the

activity of B cells.

T regulatory cells. Helper T cells secrete cytokines to enhance other immune responses, involved
in activation of both B and T cell lymphocytes
HELPER T CELLS
• Secrete cytokines (IL-2) to costimulate other T, B, and NK cells and aid in their activation.
• Involved in BOTH cell-mediated and antibody-mediated immunity
Helper T cells secrete cytokines to facilitate :

• Stimulating T cell division

• Promoting activation of B cells
• Stimulating the phagocytic activity of macrophages
• specific and nonspecific defenses and stimulate cell-mediated and antibody-mediated
immunities. Hence the name helper T cells. These cytokines stimulate T cell division that
produces memory helper cells and speeds the maturation of cytotoxic T cells. They enhance
nonspecific defenses by attracting macrophages to the affected area, preventing their
departure, and stimulating their phagocytic activity. They also attract and stimulate the
activity of cytotoxic T cells and promote the activation of B cells.
• Helper T cells are absolutely vital to the immune response, because they must activate B
cells before the B cells can produce antibodies. The reduction in the helper T cell
population that occurs in AIDS is largely responsible for the loss of immunity. 
These cytokines do the following secreted by helpr t:

Stimulate the T cell divisions that produce memory T cells and speed the maturation of
cytotoxic T cells.

Enhance nonspecific defenses by attracting macrophages to the affected area, preventing

their departure, and stimulating their phagocytic activity and effectiveness.

23
 Attract and stimulate the activity of cytotoxic T cells, providing another means of destroying
abnormal cells and pathogens.

Promote the activation of B cells, leading ultimately to antibody production.

•
•

high endothelial venules

vessels containing unique endothelial cells specialized to allow migration of lymphocytes from the
blood to the lymph node

hilum -
Contains blood vessels and nerves that enter and leave the lymph node trabecular veins - Collect blood
from small veins that merge and unite at the hilum

histamine
release by mast cells and basophils
vasoactive mediator in granules of mast cells and is the primary cause of allergies and anaphylactic
shock

It increases the degree of local inflammation and accelerates blood

flow to the region.

humoral immunity
In antibody-mediated (humoral) immunity, B cells secrete antibodies that defend against
antigens and pathogens in body fluids
I
iliac nodes-
lymphocytes
Immunity
• Immunity exhibits four general properties: specificity, versatility, memory,
and tolerance.
•
The ability to fight infection, illness, and disease
•
Two complementary mechanisms work independently and together
1. Innate (nonspecific) immunity
• Does not distinguish one type of threat from another
• Response is the same regardless of type of invading agent
• Present at birth (innate)
• Provides nonspecific resistance
• Prevents the approach, denies the entry, limits the spread of microbes
or other environmental hazards
2. Adaptive (specific) immunity
• Utilizes adaptive defenses
• Protects against particular threats
• Depends on the activities of specific lymphocytes
• Produces state of protection known as specific resistance
immediate hypersensitivity

24
 (type I) IgE-mediated mast cell degranulation caused by crosslinking of surface IgE by antigen.
• allergic rhinitis (inflammed nasal membranes) includes hay fever.

Immune surveillance
is the constant monitoring of normal tissues by NK cells sensitive to abnormal antigens
on the surfaces of cells.

 
Immunological escape is the process of a pathogen or tumor cells avoiding detection
immunocompetence,
the ability to produce an immune response after exposure to an antigen
IMMUNOCOMPETENCE:
able to carry out adaptive immune responses
- Occurs as they make several plasma proteins, including ANTIGEN RECEPTORS (molecules
capable of recognizing specific antigens)

immune responce
Lymphocytes that assist in the regulation and coordination of the immune response
are __________.
helper T and regulatory T cells
immunizations
Vaccines contain weakened or killed microbes (or parts of microbes) to activate your lymphocytes and
produce a primary response. Should you have a subsequent encounter with the living pathogen you
will have memory cells waiting to initiate a secondary response.

immunoglobulin
protein antibody; occurs as one of five main classes
1. The student cannot yet know whether she will come down with chickenpox. Her
elevated blood IgM levels indicate that she is in the early stages of a primary response to
the chickenpox virus. If her immune response proves unable to control and then eliminate
the virus, she will develop chickenpox. 2. Because chickenpox is highly contagious,
people who have not had chickenpox previously and have not been vaccinated are
susceptible to it. 3. The causative agent for chickenpox and shingles is the varicella-
zoster virus (VZV).
4. IgM antibodies are the first class of immunoglobulins secreted after an antigen is
encountered. IgG antibodies are the most common class of immunoglobulins. 5.
Antigenic specificity results from the arrangement of genes controlling the amino acid
sequences of the variable segments of antibodies. 6. Both responses involve the
production of antibodies as stimulated by antigens. The primary response develops
relatively slowly, and levels of IgG rise more slowly than do levels of IgM. The
secondary response develops much more rapidly, is more prolonged, and produces much
more IgG than IgM. 7. Any vaccine, including that for chickenpox, stimulates artificially
acquired active immunity.
During the primary response, which antibody peaks sooner? During the secondary
response, which antibody level is higher?
: During the primary response, IgM peaks sooner than IgG. During the secondary response,
the level of IgG is higher than the level of IgM.
IgA

25
 antibody whose dimer is secreted by exocrine glands, is especially effective against digestive and
respiratory pathogens, and can pass immunity to an infant through breastfeeding
IgD
class of antibody whose only known function is as a receptor on naive B cells; important in B cell
activation class of antibody is found on the plasma membrane of B cells to help in sensitization

IgE
antibody that binds to mast cells and causes antigen-specific degranulation during an allergic
response Triggers INFLAMMATION. respondsible for anaphylaxis
Sensitization to an allergen during the initial exposure leads to the production of large quantities of IgE.
Immediate hypersensitivity is a rapid and especially severe response to the presence of an antigen.
Immediate hypersensitivity is involved with which class of antibodies?
IgE

IgG
main blood antibody of late primary and early secondary responses; passed from mother to unborn
child via placenta
IgM
antibody whose monomer is a surface receptor of naive B cells; the pentamer is the FIRST antibody
made blood plasma during primary responses

IgM is the first class of antibody to be secreted in response to an antigen.  Although plasma cells
secrete these antibodies as individual IgM molecules, this class of antibodies circulates as a five-
antibody aggregate (pentamer). The concentration of IgM decreases as IgG levels increase in the
blood stream.  
The primary response first produces what class of antibodies
IgM

IgE
Sensitization to an allergen during the first exposure to that allergen activates B cells that produce
large quantities of IgE antibodies. The IgE antibodies attach to, and remain on, basophils and mast
cells throughout the body. Subsequent exposure to these same allergens leads to massive stimulation
of mast cells and basophils throughout the body, triggering widespread release of histamine and
leukotrienes. This causes the symptoms of anaphylaxis

Immunodeficiency diseases
are caused by inadequate immune responses. They may result from problems with the embryonic
development of lymphoid organs and tissue, a viral infection that depresses immune function, or
treatment with or exposure to immunosuppressive agents, such as radiation or drugs.
Immunodeficiency diseases result from (1) problems with the embryonic development of
lymphoid organs and tissues; (2) an infection with a virus, such as HIV, that depresses
immune function; or (3) treatment with, or exposure to, immunosuppressive agents, such
as radiation or drugs.

immunological memory

26
 ability of the adaptive immune response to mount a stronger and faster immune response upon re-
exposure to a pathogen
• property of adaptive immunity
• Activated lymphocytes produce two groups of cells
• Groups that attack invaders immediately
• Group that remains inactive unless exposed to the same antigen later
• These memory cells “remember” antigens, making future attacks faster, stronger, and longer-
lasting
•

inflammation
basic innate immune response characterized by heat, redness, pain, and swelling, BEGINS WITH
MAST CELL ACTIVATION
inflammatory response- Tend(s) to limit the spread of an injury or infection
Inflammation or inflammatory response
• Localized tissue response to injury producing the cardinal signs and symptoms of
inflammation
• Local redness (rubor)
• Swelling (tumor)
• Heat (calor)
• Pain (dolor)
• Sometimes lost function (functio laesa)
• Caused by various stimuli that kill cells, damage connective tissue fibers, or injure tissue
• Cause a change in chemical composition of the interstitial fluid
• Damaged cells release prostaglandins, proteins, and potassium ions
• Foreign proteins or pathogens may have been introduced
• Changes trigger complex inflammation response
Inflammation has several effects:
o The injury is temporarily repaired, and additional pathogens are prevented from
entering the wound.
o The spread of pathogens away from the injury is slowed.
o Local, regional, and systemic defenses are mobilized to overcome the pathogens and
facilitate permanent repairs. This repair process is called regeneration.
1. tissue damage, -->chemical chane in interstitial fluid
2. mast cell activation--> release of histamine and heparin from mast cells
3. A local redness, swelling, heat, and pain--> dilation of blood vessels, increased blood
flow, increased vessel permeability. --> clot formation
B. Phagocyte Attraction--> attration of phagocytes, especially neutrophils--> release of
cytokines-->[BOTH:1. removal of debris by neutrophils and macrophagesm stimulation of
fibroblasts 2. activation of specific defenses]
4. tissue repair--> pathogen removal, clot erosion, scar tissue formation

innate immunity  (NATURAL, nonspecific)

• Physical barriers
• Prevent approach of and deny access to pathogens
• Phagocytes include macrophages, NP, EP
• Remove debris and pathogens
• Immune surveillance-NK cells
• Destroys abnormal cells
• Interferons

27
 • Increase resistance of cells to viral infections
• Slow the spread of disease
• Complement system
• Attacks and breaks down surfaces of cells, bacteria, and viruses
• Attracts phagocytes
• Stimulates inflammation
• Inflammation –Heat, Redness, swelling & pain
• Fever
• Mobilizes defenses
• Accelerates repairs
• Inhibits pathogens

innate immune response

rapid but relatively nonspecific immune response
innate immune defenses include (inner)
internal antimicrobial proteins, phagocytes and natural killer cells, inflammation
and fever
Innate (Nonspecific) Immunity. The body has several physical barriers and internal
defense processes that either prevent or slow the entry of infectious organisms, or attack
them if they do enter. For example, the skin serves as a physical barrier, and phagocytes
attack invading bacteria. This type of immunity is called innate because you are born
with it, and nonspecific because it does not distinguish one potential threat from another.
Therefore, this category of immunity is called innate (nonspecific) immunity and it
depends on a class of lymphocytes called NK cells.

Innate Immunity (nonspecific):

Nonspecific because: does not involve the specific recognition of a microbe and acts against all
microbes in the same way

Attempts to prohibit microbes from accessing the body tissues and eliminate the ones that do

Innate immunity consists of a 1st and 2nd line of defense

• 1st line: Physical and chemical barriers in the skin and mucous membranes of the body
• 2nd line: Internal defenses including various cells (NK cells and phagocytes), molecules
(antimicrobial proteins), and processes (inflammation, fever)

innate vs adaptive
Innate immunity is nonspecific and does not distinguish one type of threat from
another. Adaptive immunity is specific and protects against particular threats

interferons
Interferons (IFNs)—small proteins released by cells infected with viruses—trigger the
production of antiviral proteins, which interfere with viral replication inside the cell.
IFNs are cytokines, which are chemical messengers released by tissue cells to coordinate
local activities
early induced proteins made in virally infected cells that cause nearby cells to make antiviral proteins
rise in interferons suggests viral infection

28
 Interferons (IFNs)
• A type of cytokine
• Chemical released by cells to coordinate local activities
• Released by activated lymphocytes, macrophages, and virus-infected tissues
• Trigger production of antiviral proteins in cytoplasm of nearby cells
• Do not prevent entry of viruses but interfere with viral replication
• Also stimulate activities of macrophages and NK cells

Interferon Alpha-
It attracts and stimulates NK cells, and enhances resistance to viral
infection.
interferon alpha is produced by cells infected with viruses and enhances
resistance to viral infection
Interferon alpha attracts and stimulates NK cells as a way to enhance viral resistance to viral
infection.

interferon Beta -
o secreted by fibroblasts
o It slows inflammation in a damaged area.
o Most cells other than lymphocytes and macrophages respond to viral infection by
secreting interferon beta.

interferon Gamma-

secreted by T cells and NK cells.

stimulates macrophage activity. attracts and stimulates NK cells

CHEMICAL MEDIATORS
Histamine, heparin, prostaglandins, and complement proteins
involution
After puberty, it gradually shrinks and becomes increasingly fibrous and fatty, a process called
involution.

J
The jugular trunks drain lymph from the
head and neck.

L
Lacteals

29
 Located in the small intestine; Specialized lymphatic capillaries that absorb dietary lipids, transfer
them to lymphatic vessels, and into the blood.

light chain
small protein chain of an antibody

lymph
fluid contained within the lymphatic system
lymph passes through the lymph node
1. cortex, 2. medulla, 3. hilum
Flow of lymph through a lymph node
Blood capillaries (blood) --> interstitial spaces (interstitial fluid) --> lymphatic capillaries (lymph) -->
lymphatic vessels (lymph) --> lymph nodes (lymph) --> lymphatic vessels (lymph) --> lymphatic
ducts (lymph) --> junction of the internal jugular and subclavian veins (blood)

Path of lymph through a lymph node

1. Afferent (afferens, to bring to) lymphatics
bring lymph into the node on the opposite side
from the hilum (indentation), then lymph flows:
2. Through the subcapsular space
• Network of fibers and dendritic cells (involved in immune response)
3. Into the outer cortex
• Contains B cells within germinal centers
4. Through lymph sinuses in the deep cortex
• Contains T cells
5. Into the medullary sinus at the core
• Contains B cells and plasma cells
6. Out of the lymph node in efferent (efferens, to bring out) lymphatics at the hilum and into
venous circulation

lymph node
one of the bean-shaped organs found associated with the lymphatic vessels
5. Why do lymph nodes enlarge during some infections? 

Answer: Lymph nodes enlarge during some infections because lymphocytes and phagocytes in the
nodes multiply to defend against the infectious agent.

Lymph nodes are encapsulated masses of lymphoid tissue. The paracortex is dominated by T

cells; the cortex and medulla contain B cells

Flow of lymph through a lymph node

Blood capillaries (blood) --> interstitial spaces (interstitial fluid) --> lymphatic capillaries (lymph) -->
lymphatic vessels (lymph) --> lymph nodes (lymph) --> lymphatic vessels (lymph) --> lymphatic
ducts (lymph) --> junction of the internal jugular and subclavian veins (blood)
components of a lymph node from hw: path of lymph through a node
start 1. Afferent lymphatics
2. Densritic cells

30
 3. outer cortex
4. paracortex
5. medullary sinus
6. effecerent lymphatics

lymphadenitis.
Inflammation of lymph nodes

lymphatic capillaries
smallest of the lymphatic vessels and the origin of lymph flow

LYMPHATIC DUCTS
The thoracic duct collects lymph from the body inferior to the diaphragm and from the left side of the
body superior to the diaphragm.
Blockage of lymphatic drainage produces lymphedema.
The lymphatic ducts both empty into the subclavian veins.
lymphatic system
network of lymphatic vessels, lymph nodes, and ducts that carries lymph from the tissues and back
to the bloodstream.

lymphatic trunks
large lymphatics that collect lymph from smaller lymphatic vessels and empties into the blood via
lymphatic ducts
the two large lymphatic vessels into which the lymphatic trunks empty
right lymphatic duct, and into the thoracic duct.

lymphocytes
white blood cells characterized by a large nucleus and small rim of cytoplasm
Lymphocyte production does NOT occur in THE LIVER

lymphocyte vs lymph
Lymphocytes are the primary cells of the lymphatic system. These cells respond to
pathogens, abnormal body cells, and foreign proteins such as toxins released by some
bacteria. Lymph is the interstitial fluid that has entered a lymphatic vessel.

New lymphocytes are produced in the germinal center of a lymph node.

Lymphedema
• Caused by blocked lymphatic drainage
• Interstitial fluids accumulate
• Affected area becomes swollen and distended
• Most often seen in limbs, but can affect other areas
• Swelling may become permanent
• Connective tissue loses elasticity
• Stagnant interstitial fluids may accumulate toxins and pathogens
• Local immune defenses overwhelmed
lymphoid nodules

31
 unencapsulated patches of lymphoid tissue found throughout the body

Lymphotoxin-
Secreted compound that disrupts cell metabolism

lymphatic vessels
Lymphatic vessels transport lymph from peripheral tissues to the venous system.

lymphopoiesis
involves the red bone marrow, thymus, and peripheral lymphoid tissues.
Lymphopoiesis (lymphocyte production)
• Involves:
• Red bone marrow
• Thymus
• Peripheral lymphoid tissues
• Red bone marrow plays the primary role in maintaining the normal lymphocyte population
• Hematopoietic stem cells here produce lymphoid stem cells

M
macrophage
ameboid phagocyte found in several tissues throughout the body

macrophage oxidative metabolism

metabolism turned on in macrophages by T cell signals that help destroy intracellular bacteria

major histocompatibility complex (MHC)

• molecules; "self-antigens" located in the plasma membrane of body cells.
• gene cluster whose proteins present antigens to T cells

mast cell
cell found in the skin and the lining of body cells that contains cytoplasmic granules with vasoactive
mediators such as histamine

MAST CELLS Stimulation and coordination of inflammation by releasing histamine and heparin

MAST CELLS:
INCREASE blood flow
activate complement
activate macrophages

When stimulated by physical stress or chemical changes in the local environment, mast cells release
histamine, heparin, prostaglandins, and other chemicals into interstitial fluid.
histamine makes capillaries more permeable and speeds up blood flow through the area. The combination
of abnormal tissue conditions and chemicals released by mast cells stimulates local sensory neurons,
producing pain. The person then may take steps to limit the damage, such as removing a splinter or
cleaning a wound.

Medullary sinus-
Contains B cells and plasma cells

32
MEMORY B CELLS
Memory B cells perform the same role in antibody-mediated immunity that memory T
cells perform in cell-mediated immunity. Memory B cells do not respond to a threat on
first exposure. Instead, they remain in reserve to deal with subsequent injuries or
infections that involve the same antigens. On subsequent exposure, the memory B cells
divide and differentiate into plasma cells that secrete antibodies in massive quantities.
memory T cells
respond to antigens they have already encountered by the cloning (producing identical
cellular copies) of more lymphocytes to ward off the invader.
long-lived immune cell reserved for future exposure to an pathogen Memory TC cells Cells that
do not differentiate further the first time the antigen triggers an immune response
The interplay between helper T cells and regulatory T cells helps establish and control the
sensitivity of the immune response.

MESENTERIC nodes
are important in removing pathogens that have entered through thesmall intestines

MHC class I
found on most cells of the body, it binds to the CD8 molecule on T cells
When any body cell is infected with a viral or bacterial pathogen, abnormal peptides are present in the
infected cell’s cytoplasm. The abnormal peptides are incorporated into the cell’s normal class I MHC
proteins. These MHC proteins with the attached abnormal peptides are moved to the plasma
membrane by transport vesicles and become part of the plasma membrane. As a result, the body cell
then displays abnormal peptides on its membrane and functions as an antigen-presenting cell.
Memory Tc cells:
are produced by the thousands, but they do not differentiate further the first time the antigen triggers an
immune response.

MHC class II
found on macrophages, dendritic cells, and B cells, it binds to CD4 molecules on T cells

MHC polygeny
multiple MHC genes and their proteins found in body cells

MHC polymorphism
multiple alleles for each individual MHC locus

monocyte
precursor to macrophages and dendritic cells seen in the blood

mucosa-associated lymphoid tissue (MALT)

lymphoid nodule associated with the mucosa
Mucosa-associated lymphoid tissue (MALT) is found in the digestive tract, reproductive tract and
urinary system

33
N
naïve lymphocyte
mature B or T cell that has not yet encountered antigen for the first time

natural killer cell (NK)

 large granular lymphocytes) 

cytotoxic lymphocyte of innate immune response

Cytotoxic T cells and NK cells can be activated by direct contact with virus-infected
cells.
NK cells recognize cancer cells by the tumor-specific antigens on the plasma membranes
of cancer cells
How do NK cells detect cancer cells? (Module 20.11B)

1. Presence of unusual plasma membrane activates Natural Killer Cells

2. NK cells adheres to target cell, release perforins which perforate cell, it dies

Steps of NK recognition and destruction

1. Presence of unusual plasma membrane activates NK cell
• NK cell adheres to target cell
2. Golgi apparatus moves within NK cell near target cell
• Produces many secretory vesicles containing perforins
3. Perforins released from NK cell and arrive at target cell
4. Perforins create pores in target cell membrane
• Target cell can no longer maintain its internal environment and disintegrates
1) Recognition and Adhesion. If a cell has unusual components in its plasma membrane, an
NK cell recognizes that cell as abnormal. This recognition activates the NK cell, which
then adheres to its target cell.
2) Realignment of Golgi Apparatus. The Golgi apparatus moves around the nucleus until
the maturing (trans) face points directly toward the abnormal cell. The process might be
compared to the rotation of a tank turret to point the cannon toward the enemy. The Golgi
apparatus then produces a flood of secretory vesicles that contain proteins
called perforins. These vesicles move through the cytosol toward the cell surface.
3) Secretion of Perforin. The perforins are released at the NK cell surface by exocytosis
and diffuse across the narrow gap between the NK cell and its target.
4) Lysis of Abnormal Cell. When perforin molecules reach the opposing plasma
membrane, the perforins interact with one another and create a network of pores in it.
These pores are large enough to allow the free passage of ions, proteins, and other
intracellular materials. As a result, the target cell can no longer maintain its internal
environment, and it quickly disintegrates.

Naturally acquired active immunity-

type of immunity develops after exposure to antigens in the environment

Necrosis
is tissue or cell death after injury.

34
negative selection
selection against thymocytes in the thymus that react with self-antigen

neutralization
inactivation of a virus by the binding of specific antibody

neutrophil
phagocytic white blood cell recruited from the bloodstream to the site of infection via the
bloodstream
After neutrophils are drawn to an area and they attack debris and bacteria, they undergo activation.
released when neutrophils are activated:
 Neutrophils, once activated, do release hydrogen peroxide and nitric oxide as part of their respiratory
burst. Neutrophils also release cytokines to draw more neutrophils to the site of the infection

• leukocytes are abundant, mobile, and quick to phagocytize cellular debris or invading
bacteri

O
opsonization
a coating of antibodies and complement proteins on the surface of a pathogen increases the
effectiveness of phagocytosis.
The attachment of C3b enhances phagocytosis, a process
called opsonization. 

P
paracortex
(DEEP CORTEXT) lymph node structure is dominated by T cells
passive immunity
Passive immunity is produced by transferring antibodies from another source

transfer of immunity to a pathogen to an individual that lacks immunity to this pathogen usually by
the injection of antibodies
passive immunity Produced by the transfer of antibodies from another
source
What type of immunity is conferred when a baby receives antibodies from her
mother?
Naturally acquired passive immunity

Because the baby is being given antibodies, this is passive immunity. This is, of
course, a natural way of conferring antibodies. Antibodies cross the placenta or
are given through the milk in breastfeeding. So this is naturally acquired
passive immunity.

35
Passive immunity
Produced by the transfer of antibodies from another source
• Naturally acquired
• Example: transfer of maternal antibodies across placenta or breast milk
• Artificially induced
• Example: administration of antibodies to a patient
• In passive immunity, antibodies are introduced into the body by
injection. Because these antibodies were produced not inside the body
but by an outside source, this is termed a “passive process.” This is in
contrast to active immunity, which means that the body’s tissues are
doing work in order to produce proteins known as antibodies to
counteract a foreign antigen. The antigen is then neutralized as it is
directly bound to the antibody.
pattern recognition receptor (PRR)
leukocyte receptor that binds to specific cell wall components of different bacterial species

perforin
molecule in NK cell and cytotoxic T cell granules that form pores in the membrane of a target cell
perforins-
Vesicular proteins that interact to create a network of pores

peripheral tolerance
mature B cell made tolerant by lack of T cell help

Peyer's patches
aggregated lymphoid nodules that contains the germinal center where lymphocytes divid

phagocytosis
movement of material from the outside to the inside of the cells via vesicles made from
invaginations of the plasma membrane

plasma cell
differentiated B cell that is actively secreting antibody
an elevated number of plasma cells in the lymph would lead you to expect higher-than-normal
antibody levels in the blood.
Plasma cell is the name for the type of B cell that synthesizes and secretes large
quantities of antibodies. This cell results from a B cell which has bound a specific
antigen, causing activation and differentiation of the B cell into a dedicated cell
producing specific antibody that binds the antigen and inactivates it. 

polyclonal response
response by multiple clones to a complex antigen with many determinants

positive selection
selection of thymocytes within the thymus that interact with self, but not non-self, MHC molecules

36
primary adaptive response
immune system’s response to the first exposure to a pathogen
The primary response takes time to develop because the antigen must activate the appropriate B
cells. These cells must then differentiate into plasma cells. As plasma cells differentiate and
begin secreting, the concentration of circulating antibodies makes a gradual, sustained ris
During the primary response, IgM peaks sooner than IgG. During the secondary response, the level
of IgG is higher than the level of IgM.
During the primary response, the antibody titer, or level of antibodies in the plasma, does not
peak until 1 to 2 weeks after the initial exposure. If the person is no longer exposed to the
antigen, the antibody concentration then declines. The antibody titer declines because (1) plasma
cells have very high metabolic rates and survive for only a short time, and (2) regulatory T cells
release suppression factors that inhibit further production of plasma cells. However, regulatory T
cell activity does not begin immediately after exposure to the antigen. Also, under normal
conditions helper T cells outnumber regulatory T cells by more than 3 to 1. As a result, many B
cells are activated before regulatory T cell activity has a noticeable effect.

primary lymphoid organ

site where lymphocytes mature and proliferate; red bone marrow and thymus gland

properdin-
It is a complement protein that initiates the alternative pathway when
it interacts with other complement proteins in the plasma.
psychoneuroimmunology
study of the connections between the immune, nervous, and endocrine systems
pulp
WHITE PULP
white pulp- Resembles lymphoid nodules, CONTAINS LYMPHOCYTES,
purple because nucli of lymphocytes stain darker
white pulp= periarteriolar lymphocyte sheath
white pulp has a high concentration of lymphocytes and dendritic cells

blood supplied to the red pulp by the venous sinuses

 a network of reticular fibers.
The blood passes through this meshwork and enters large sinusoids, also lined by fixed macrophages.
The sinusoids empty into small veins, which ultimately collect into trabecular veins that continue
toward the hilum.

Macrophages are scattered throughout the red pulp, and the area surrounding the white pulp has a high
concentration of lymphocytes and dendritic cells. For this reason, any microorganism or other antigen
in the blood quickly triggers an immune response.

RED PULP
• In the spleen, the network of blood sinusoids is called the red pulp.
• red pulp =splenic cords
• blood supplied to the red pulp by the venous sinuses
• cell population includes all the normal components of circulating blood, plus
fixed and free macrophages. 

37
 • Structural framework of the red pulp consists of a network of reticular fibers. The
blood passes through this meshwork and enters large sinusoids, also lined by
fixed macrophages. The sinusoids empty into small veins, which ultimately
collect into trabecular veins that continue toward the hilum.
This circulatory arrangement gives the phagocytes in the spleen an opportunity to identify and
engulf damaged or infected cells in circulating blood. Macrophages are scattered throughout
the red pulp, and the area surrounding the white pulp has a high concentration of lymphocytes
and dendritic cells. For this reason, any microorganism or other antigen in the blood quickly
triggers an immune response.

Pyrogens
Pyrogens increase body temperature (produce a fever) by stimulating the temperature
control area of the pre-optic nucleus of the hypothalamus.
increase body temperature (produce a fever), which can mobilize defenses, accelerate
repairs, and inhibit pathogens.
high levels of Pyrogens indicate fever
Bacteria, molds, viruses, and yeasts produce pyrogens and release them into the
bloodstream. Several endogenous, or internally produced, pyrogens have been identified
including interleukin-1, interferons, and tumor necrosis factor.

R
red bone marrow
8. What types of cells would be affected by a decrease in the number of monocyte-forming cells in red bone
marrow? 

Answer: A decrease in the number of monocyte-forming cells in red bone marrow would result in fewer
macrophages of all types, including stellate macrophages (Kupffer cells) of the liver, microglia of the central
nervous system, and alveolar macrophages.
regulatory T cells (Treg)
(also, suppressor T cells) class of CD4 T cells that regulates other T cell responses
are a subset of T cells that moderate the immune response.

respiratory burst
refers to the reactive compounds released by activated neutrophils.
Regulatory T cells, referred to as T , moderate the responses of other T cells and of B
regs

cells by secreting inhibitory cytokines called suppression factors. Suppression does not

take place right away, because activation takes much longer for regulatory T cells than
for other types of T cells. In addition, upon activation, most of the CD8 T cells in the
bloodstream produce cytotoxic T cells rather than regulatory T cells. As a result,
regulatory T cells act after the initial immune response. In effect, these cells limit the
degree of immune system activation from a single stimulus.

38
Rheumatoid arthritis
autoantibodies attack connective tissues around joints

right lymphatic duct

drains lymph fluid from the upper right side of body into the right subclavian vein
right lymphatic duct collects lymph from the right side of the body superior to the diaphragm
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the lower
limbs by way of the right and left lumbar trunks and the intestinal trunk
The right lymphatic duct is formed by the merging of the right jugular, right subclavian,
and right bronchomediastinal trunks in the area near the right clavicle. This duct empties into
the right subclavian vein, delivering lymph from the right side of the body superior to the
diaphragm

S
secondary adaptive response
immune response observed upon re-exposure to a pathogen, which is stronger and faster than a
primary response
During the initial exposure to a new antigen, a naïve B cell will take up to several weeks to produce
enough antibody to mount a sufficient immune response. On a second exposure, however, because of
the memory cells that were saved and stored from the first exposure, the time frame for antibody titers
(levels) to rise is much shorter. The immune system is already primed and ready to be triggered into a
fast response because of this cellular memory.
The primary response develops relatively slowly, and levels of IgG rise more slowly than do
levels of IgM.
The secondary response develops much more rapidly, is more prolonged, and produces much
more IgG than IgM.

 
• It inhibits the formation of an infection.
• It produces a large amount of IgG.
• It is caused by memory B cells.
• Begins almost immediately (less than one week)  
• Massive antibody response  
• NOT IgM levels much higher than IgG levels. 

•
• Unless memory B cells are exposed to the same antigen a second time, they do not differentiate into plasma
cells. If and when that exposure occurs, the memory B cells respond right away—faster than the B cells
stimulated during the initial exposure. This response is immediate in part because memory B cells are
activated at relatively low antigen concentrations. In addition, these cells synthesize more effective and
destructive antibodies. Activated memory B cells divide and differentiate into plasma cells that secrete these
antibodies in massive quantities. This secretion is the secondary response to antigen exposure.
• During the secondary response, antibody concentrations and titers increase more rapidly and reach levels
many times higher than they did in the primary response (Figure 22–25b). The secondary response appears
even if the second exposure occurs years after the first. The reason is that memory cells may survive for 20
years or more.

39
 The primary response develops slowly and does not produce antibodies in massive quantities.
For these reasons, it may not prevent an infection the first time a pathogen appears in the
body. However, a person who survives the first infection will probably be resistant to that
pathogen in the future, thanks to a rapid and overwhelming secondary response. The
effectiveness of the secondary response is one of the basic principles behind the use of
immunization to prevent disease.
WHICHh would be more negatively affected—the primary response or the secondary response—by a
lack of memory B cells for a particular antigen? 
Answer: Because production of a secondary response depends on the presence of memory B cells and
memory T cells formed during a primary response, the secondary response would be more negatively
affected by a lack of memory B cells for a particular antigen.
•
•

secondary lymphoid organs

sites where lymphocytes mount adaptive immune responses; examples include lymph nodes and
spleen
sensitization
first exposure to an antigen When binding occurs, the B cell prepares to undergo activation. This
preparatory process is called sensitization 
: Sensitization is the process by which a B cell becomes able to react with a specific antigen.

seroconversion
clearance of pathogen in the serum and the simultaneous rise of serum antibody
severe combined immunodeficiency disease (SCID)
genetic mutation that affects both T cell and B cell arms of the immune response

sinusoids
contain fixed macrophages
Specificity
property of adaptive immunity
T cells and B cells have receptors for only one specific antigen
Responses of activated T cell or B cell are also specific (do not affect any other antigens)
spleen
- largest single collection of lymphoid tissue, FRAGILE AND DIFFICULT TO
REPAIR
-secondary lymphoid organ that filters pathogens from the blood (white pulp) and removes
degenerating or damaged blood cells (red pulp)
Red pulp
contains large numbers of red blood cells;

white pulp resembles lymphoid nodules and contains lymphocytes.

In the spleen, the network of blood sinusoids is called the red pulp.

The spleen is surrounded by a capsule containing collagen and elastic fibers. The cellular components
within make up the pulp of the spleen (Figure 22–8c). Red pulp contains large quantities of red blood
cells, and white pulp resembles lymphoid nodules. Interestingly, the spleens of dogs, cats, and other
mammals have extensive smooth muscle layers that contract to eject blood into the bloodstream. The
human spleen lacks these muscles and therefore cannot contract.

40
 The splenic artery enters at the hilum and branches to produce a number of arteries that radiate
outward toward the capsule.
This circulatory arrangement gives the phagocytes in the spleen an opportunity to identify and
engulf damaged or infected cells in circulating blood. Macrophages are scattered throughout
the red pulp, and the area surrounding the white pulp has a high concentration of lymphocytes and
dendritic cells. For this reason, any microorganism or other antigen in the blood quickly triggers an
immune response.

sinusoids
contain fixed macrophages

Suppressor T cells (TS cells):

Inhibit the activation and function of both T cells and B cells
Suppressor T cells (TS cells):act only after the initial immune response.

T
T cell
lymphocyte that acts by secreting molecules that regulate the immune system or by causing the
destruction of foreign cells, viruses, and cancer cells
• Cell-mediated defenses (T cells)
• 80% of lymphocytes
All T cells have a CD3 receptor complex in their plasma membranes, and this complex ultimately activates the
T cell. Either of two other CD markers may be bound to the CD3 receptor complex, and these two CD markers
are especially important in specific groups of T cells:
 CD8 markers are found on cytotoxic T cells and regulatory T cells, which together are often called CD8 T
cells. CD8 T cells respond to antigens presented by class I MHC proteins.
 CD4 markers are found on helper T cells, often called CD4 T cells. CD4 T cells respond to antigens
presented by class II MHC proteins.

T cells are not usually activated upon their first encounter with the antigen. Antigen recognition simply prepares
the cell for activation.

T cell tolerance
process during T cell differentiation where most T cells that recognize antigens from one’s own body
are destroyed

T cell-dependent antigen
antigen that binds to B cells, which requires signals from T cells to make antibody

T cell-independent antigen
binds to B cells, which do not require signals from T cells to make antibody

Th1 cells

41
 cells that secrete cytokines that enhance the activity of macrophages and other cells

Th2 cells
cells that secrete cytokines that induce B cells to differentiate into antibody-secreting plasma cells

Thoracic Duct
Which region of the body is drained by the THORACIC duct?
LEFT ARM.
thoratic duct drains into left brachiocephalic vein

large duct that drains lymph from the lower limbs, left thorax, left upper limb, and the left side of the
head
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the lower
limbs by way of the right and left lumbar trunks and the intestinal trunk

 The thoracic duct collects lymph from the body inferior to the diaphragm and from the left side of the
body superior to the diaphragm. 

lab?: thoratic duct drains into left brachiocephalic vein

It collects lymph from the left bronchomediastinal trunk, the left subclavian trunk, and
the left jugular trunk, and then empties into the left subclavian vein near the left internal
jugular vein
right lympatic duct empties lymph into right subclavian vein

thoratic duct drains into left brachiocephalic vein

right lymphatic duct collects lymph from the right side of the body superior to the diaphragm
The cisterna chyli receives lymph from the inferior part of the abdomen, the pelvis, and the lower
limbs by way of the right and left lumbar trunks and the intestinal trunk
The right lymphatic duct is formed by the merging of the right jugular, right subclavian,
and right bronchomediastinal trunks in the area near the right clavicle. This duct empties into
the right subclavian vein, delivering lymph from the right side of the body superior to the
diaphragm
How would blockage of the thoracic duct affect lymph circulation? 

Answer: A blockage of the thoracic duct would impair the drainage of lymph from inferior to
the diaphragm and from the left side of the head and thorax, slowing the return of lymph to
the venous blood and promoting the accumulation of fluid in the limbs (lymphedema).

thymic (Hassall’s) corpuscles

The epithelial reticular cells in the medulla cluster together in concentric layers

thymocyte
immature T cell found in the thymus

thymus
primary lymphoid organ; where T lymphocytes proliferate and mature

42
 Cortex -contains actively dividing T cell lymphocytes (T lymphocytes).
Epithelial reticular cells maintain the blood thymus barrier around the blood vessels of
the cortex, which separates developing T cells from the general circulation.
These epithelial cells also regulate T cell development and function.
medulla-
Maturing T cells leave the cortex and enter the medulla of the thymus. The medulla has
no blood thymus barrier. After about 3 weeks, these T cells leave the thymus by entering
one of the medullary blood vessels. T cells in the medulla can enter or leave the
bloodstream across the walls of blood vessels in this region or within one of the efferent
lymphatics that collect lymph from the thymus.

Thymosin
hormone from the thymus that promotes the development and maturation of T cells. 
 
Thyroiditis
inflammation resulting from autoantibodies attacking thyroglobulin

tissue typing
typing of MHC molecules between a recipient and donor for use in a potential transplantation
procedure

Tolerance
property of adaptive immunity
• Immune response ignores “self” but targets abnormal and foreign “non-self” cells and toxins
• Can develop over time in response to chronic exposure to an antigen

tonsils
The role of the tonsils is to protect the upper respiratory and digestive tracts from infections

lymphoid nodules associated with the nasopharynx

lingual tonsil- Trap bacteria and viruses

Palatine-usually the tonsil(s) removed in a tonsillectomy

PHARYNGEAL TONSIL- adenoid

• Pharyngeal tonsil (or the adenoid)

• Located on posterior superior wall of the nasopharynx
• Palatine tonsils (left and right)
• Located at posterior, inferior margin of the oral cavity along the boundary of
the pharynx
• Lingual tonsils
• Pair of tonsils located deep to the epithelium covering the base of the tongue

Which of the following may occur as a result of removal of the palatine or pharyngeal tonsils?
heightened susceptibility to ingested or inhaled pathogens

43
 A patient visits her doctor for a routine checkup. The doctor observes lymphadenopathy, or
swollen lymph nodes in the side of the patient's neck. The patient says, "Those have been
swollen for a few months, but I have felt fine that whole time." Indeed there are no other
symptoms. What is a likely cause of this problem?
The patient is HIV positive.
TONSILS AND SPLEEN do NOT display the outer cortex/inner medulla pattern?

Trabeculae
- Fibrous partitions that extend inward from the capsule

trabecular veins
- Collect blood from small veins that merge and unite at the hilum

trabecular arteries
- Branches of the splenic artery

Tracheobronchial nodes
filter lymph from bronchi and trachea

type I hypersensitivity
immediate response mediated by mast cell degranulation caused by the crosslinking of the antigen-
specific IgE molecules on the mast cell surface

type II hypersensitivity
cell damage caused by the binding of antibody and the activation of complement, usually against red
blood cells

type III hypersensitivity

damage to tissues caused by the deposition of antibody-antigen (immune) complexes followed by
the activation of complement

VACCINE
 A vaccine, containing weakened or dead forms of the infecting microbe (antigen), is
administered orally, intranasally, subcutaneously, or intramuscularly. The antigens are
not virulent enough to cause the disease, but they provoke the adaptive immune response
in the body. This immune response involves B cells that differentiate into plasma cells
and make antibodies. It also involves cytotoxic T cells and helper T cells. Regulatory T
cells moderate the immune response. Memory T cells and memory B cells help the body
remember the antigen so when the protected person is exposed to the real disease, a
strong secondary immune response occurs.

Vaccinations are as varied as the diseases they protect against. Some are given as live,
attenuated (greatly weakened) forms of a virus. Others are given as inactivated antigens,
made from small pieces of killed bacteria. Some vaccines require repeat doses (booster
shots) to boost the secondary immune response and keep immune memory alive.

44
1. Is immunity to chickenpox, developed after vaccination, innate immunity, or adaptive immunity?
Why? 

Answer: Innate immunity is genetically determined and present at birth. For example, skin and
mucous membranes provide an innate physical and chemical barrier to infecting organisms. All
humans are susceptible to chickenpox, an infectious disease. The immunity developed after a
chickenpox vaccination is artificially acquired adaptive immunity, developed to a specific antigen,
the varicella- zoster virus (VZV).
variable region domain
part of a lymphocyte antigen receptor that varies considerably between different receptor types

Versatility
property of adaptive immunity
Millions of lymphocytes, each sensitive to a different antigen
When activated, a lymphocyte divides
Produces more lymphocytes with same specificity

white pulp- Resembles lymphoid nodules

white pulp= periarteriolar lymphocyte sheath

Difference between B and T lymphocytes with regard to their origin, maturation into
immunocompetent cells, and general function
• T cells and B cells are lymphocytes that both develop from stem cells in the red bone
marrow
• B cells complete development in the red bone marrow
• T cells complete their development in the thymus
Mature T cells include: Helper T cells and cytotoxic T cells

• Both become immunocompetent before entering the bloodstream

IMMUNOCOMPETENCE: able to carry out adaptive immune responses

- Occurs as they make several plasma proteins, including ANTIGEN RECEPTORS
(molecules capable of recognizing specific antigens)

The ______ collects the urine produced by a single kidney lobe.

minor calyx

Which nervous system structure(s) inhibits micturition by relaxing the detrusor and contracting the internal
urethral sphincter?
Stretch receptor impulses activate sympathetic outflow

Formation of angiotensin I is triggered by ______.

renin

45
Which structure is composed of a layer of collagen fibers that covers the entire outer surface of the
kidney?
fibrous capsule

Part complete
What is the function of the vasa recta?

to collect and transport water and solutes within the renal medulla in association with the juxtamedullary
nephron

Variable secretion of potassium and hydrogen ions is a specific function of which renal structure?
collecting system

Which renal structure begins in the renal cortex and carries tubular fluid through the osmotic gradient in
the renal medulla?
collecting duct

Contraction of which structure compresses the urinary bladder and expels its contents into the urethra?
detrusor muscle

Which event correctly occurs under maximum ADH stimulation?

The DCT and collecting system become more permeable to water.

The ______ control(s) capillary diameter and the rate of capillary blood flow.
mesangial cells

Filtration in the Nephron:

Which structure filters the blood?
renal corpuscle
In the renal corpuscle, blood pressure pushes fluid out of the glomerulus and into the glomerular capsule.
This initial filtrate is similar to plasma, lacking only the large plasma proteins. The rest of the nephron and
collecting system will carry out reabsorption and secretion to adjust the volume and content of the filtrat

In which portion of the nephron and collecting system does the most reabsorption occur?
proximal convoluted tubule
The proximal convoluted tubule reabsorbs 60–70 percent of the water and ions from the filtrate, plus 99–
100 percent of organic solutes such as glucose. This reduces the volume of the filtrate from 180 L/day to
between 64 and 72 L/day. The rest of the nephron and collecting system will further reduce the filtrate to
the average urine volume of 1.8 L/day.

The nephron loops of juxtamedullary nephrons have an important function that other parts of the
nephron do not share. What is this function?

establishing the concentration gradient in the renal medulla

The nephron loops work to keep the renal medulla hypertonic to the plasma. This concentration gradient
will be essential to water reabsorption in the collecting duct.

Different parts of the nephron and collecting system cooperate to carry out the three processes of urine
formation. Filtration occurs only in the renal corpuscle; the tubules and collecting duct reabsorb and

46
secrete to adjust the volume and content of the filtrate to turn it into urine. The details of these processes
are discussed in the remaining modules of Section 2.

When the pH of body fluids decreases, which of the following are secreted in exchange for sodium ions
reabsorbed in the distal convoluted tubule?
hydrogen ions

47
48
Actions of Antibodies
The formation of an antigen–antibody complex may cause the elimination of the antigen in the
following ways:

 Neutralization. Both viruses and bacterial toxins have specific sites that must bind to
target regions on body cells before they can enter or injure those cells. Antibodies may bind
to those sites, making the virus or toxin incapable of attaching itself to a cell. This
mechanism is known as neutralization.
 Precipitation and Agglutination.  Each antibody molecule has two antigen-binding sites,
and most antigens have many antigenic determinant sites. If individual antigens (such as
macromolecules or bacterial cells) are far apart, an antibody molecule will necessarily bind
to two antigenic sites on the same antigen. However, if antigens are close together, an
antibody can bind to antigenic determinant sites on two separate antigens. In this way,
antibodies can link large numbers of antigens together. The three-dimensional structure
created by such binding is known as an immune complex. When the antigen is a soluble
molecule, such as a toxin, this process may create complexes that are too large to remain in
solution. The formation of insoluble immune complexes is called precipitation. When the
target antigen is on the surface of a cell or virus, the formation of large complexes is
called agglutination. We discussed an example of agglutination with the clumping of
erythrocytes that occurs when incompatible blood types are mixed. p. (669)
 Activation of the Complement System.  When an antibody molecule binds to an antigen,
portions of the antibody molecule change shape. This change exposes areas that bind
complement proteins. The bound complement molecules then activate the complement
system, which destroys the antigen (as discussed previously).

 Attraction of Phagocytes. Antigens covered with antibodies attract eosinophils,

neutrophils, and macrophages. These cells phagocytize pathogens and destroy foreign or
abnormal plasma membranes.

 Opsonization.  A coating of antibodies and complement proteins increases the

effectiveness of phagocytosis. This effect is called opsonization. Some bacteria have slick
plasma membranes or capsules, but opsonization makes it easier for phagocytes to hold onto
their prey before they engulf it. Phagocytes can bind more easily to antibodies and
complement proteins than they can to the bare surface of a pathogen.

49
  Stimulation of Inflammation. Antibodies may promote inflammation by stimulating
basophils and mast cells.

 Prevention of Bacterial and Viral Adhesion. Antibodies dissolved in saliva, mucus, and

perspiration coat epithelia, adding an additional layer of defense. A covering of antibodies
makes it difficult for pathogens to attach to and penetrate body surfaces.

Stress and the Immune Response

One of the normal effects of interleukin-1 secretion is the stimulation of adrenocorticotropic
hormone (ACTH) production by the anterior lobe of the pituitary gland. This hormone in turn
prompts the secretion of glucocorticoids by the adrenal cortex. p. 636 The anti-inflammatory
effects of the glucocorticoids may help control the extent of the immune response.
However, chronic stress depresses the immune system and can be a serious threat to health. The
long-term secretion of glucocorticoids, as in the resistance phase of the stress response, can
inhibit the immune response and lower a person’s resistance to disease. p. 648 The effects of
glucocorticoids that alter the effectiveness of innate and adaptive defenses include the following:
 Depression of Inflammation. Glucocorticoids inhibit mast cells and make capillaries less
permeable. Inflammation becomes less likely. When it does occur, the reduced permeability
of the capillaries slows the entry of fibrinogen, complement proteins, and cellular defenders
into tissues.

 Reduction in the Abundance and Activity of Phagocytes in Peripheral

Tissues. This reduction further impairs innate defense mechanisms. It also interferes with
the processing and presentation of antigens to lymphocytes.

 Inhibition of Interleukin Secretion. A reduction in interleukin production depresses the

response of lymphocytes, even to antigens bound to MHC proteins.

The mechanisms that bring about these changes are still under investigation.

50
Immune Disorders
Because the immune response is so complex, many opportunities exist for things to go wrong. A
variety of clinical conditions result from disorders of the immune function. A common class of
immune disorders is allergies, also called hypersensitivities. Autoimmune disorders develop
when the immune response inappropriately targets normal body cells and tissues. In
an immunodeficiency disease, either the immune system fails to develop normally or the immune
response is blocked in some way. Autoimmune disorders and immunodeficiency diseases are
fairly rare—clear evidence of the effectiveness of the immune system’s control mechanisms.

Hypersensitivities
Hypersensitivities, commonly called allergies, are excessive immune responses to antigens. The
sudden increase in cellular activity or antibody titers can have several unpleasant side effects.
For example, neutrophils or cytotoxic T cells may destroy normal cells while they are attacking
an antigen. Or the antigen–antibody complex may trigger massive inflammation. Antigens that
set off allergic reactions are often called allergens.
There are several types of hypersensitivities. A complete classification has four
categories: immediate hypersensitivity (type I), cytotoxic reactions (type II), immune complex
disorders (type III), and delayed hypersensitivity (type IV). In Chapter 19 we discussed one
example of a cytotoxic (type II) reaction: the cross-reaction that follows the transfusion of an
incompatible blood type. p. 669 Here we focus on immediate hypersensitivity (type I). It is
probably the most common type of allergy.
Immediate hypersensitivity is a rapid and especially severe response to an antigen. One
form, allergic rhinitis, includes hay fever and environmental allergies. This form may affect 15
percent of the U.S. population. Sensitization to an allergen during the initial exposure leads to the
production of large quantities of IgE. Genes may determine a person’s tendency to produce IgE
in response to particular allergens.
Due to the lag time needed to activate B cells, produce plasma cells, and synthesize antibodies,
the first exposure to an allergen does not produce signs and symptoms. Instead, it sets the stage
for the next encounter. After sensitization, the IgE molecules become attached to basophils and
mast cells throughout the body. When the individual meets the same allergen again, the bound
antibodies stimulate these cells to release histamine, heparin, several cytokines, prostaglandins,
and other chemicals into the surrounding tissues. This results in a sudden, massive inflammation
of the affected tissues.

The cytokines and other mast cell secretions draw basophils, eosinophils, T cells, and
macrophages into the area. These cells release their own chemicals, extending and intensifying
the responses initiated by mast cells. The severity of the allergic reaction depends on the
individual’s sensitivity and on the location involved. If allergen exposure occurs at the body
surface, the response may be restricted to that area. If the allergen enters the bloodstream, the
response could be lethal.

In anaphylaxis (an-uh-fuh-LAK-sis; ana-, again + phylaxis, protection), a circulating allergen

affects mast cells throughout the body (Figure 22–29). In drug reactions, such as allergies to
51
penicillin, IgE antibodies are produced in response to a hapten (partial antigen) bound to a larger
molecule that is widely distributed within the body because the combination acts as an allergen.
A wide range of signs and symptoms can develop within minutes. Changes in capillary
permeabilities produce swelling and edema in the dermis, and raised welts, or hives, appear on
the skin. Smooth muscles along the respiratory passageways contract, and the narrowed passages
make breathing extremely difficult. In severe cases, an extensive peripheral vasodilation occurs,
producing a drop in blood pressure that can lead to a circulatory collapse. This response
is anaphylactic shock.

22. Which kind of immunity protects a developing fetus, and how is that immunity produced? 

Answer: A developing fetus is protected primarily by naturally acquired passive immunity, through
the maternal production of IgG antibodies that have crossed the placenta from the mother’s
bloodstream
3. How does increased stress reduce the effectiveness of the immune response? 

Answer: Stress can interfere with the immune response by depressing inflammation, reducing the
number and activity of phagocytes, and inhibiting interleukin secretion.
24. Define autoimmune disorder. 

Answer: An autoimmune disorder is a condition that results when the immune system’s sensitivity to
normal cells and tissues causes the production of autoantibodies

AGING
T cells become less responsive to antigens, so fewer cytotoxic T cells respond to an infection.
This effect may be due to the gradual decrease in the size of functional tissue and secretory
abilities of the thymus and to lower circulating levels of thymic hormones. Because the number
of helper T cells is also reduced, B cells are less responsive, so antibody levels do not rise as
quickly after antigen exposure. The net result is an increased susceptibility to viral and bacterial
infections. For this reason, vaccinations for acute viral diseases such as the flu (influenza), and
for pneumococcal pneumonia, are strongly recommended for elderly individuals. The increased
incidence of cancer in elderly people reflects the fact that immune surveillance declines, so
tumor cells are not eliminated as effectively.
25. Why are elderly people more susceptible to viral and bacterial infections? 

Answer: Elderly people are more susceptible to viral and bacterial infections because the number of
helper T cells declines with age and B cells are less responsive, so antibody levels rise more slowly
after antigen exposure.

26. What may account for the increased incidence of cancer among elderly people? 

Answer: As one ages, immune surveillance declines, so cancerous cells are not eliminated as
effectively.

52
LYMPHATIC SYSTEM AND INTERACTIONS WITH OTHER BODY SYSTEMS
 The thymus secretes oxytocin, ADH, and endorphins as well as thymic hormones. The
effects on the CNS are not known, but removal of the thymus lowers brain endorphin levels.
 Both thymic hormones and cytokines help establish the normal levels of CRH and TRH
produced by the hypothalamus.
 Other thymic hormones affect the anterior lobe of the pituitary gland directly, stimulating
the secretion of prolactin and GH.
 27. What is the relationship between the endocrine system and the lymphatic system? 


 Answer: Glucocorticoids released by the endocrine system have anti-inflammatory effects;

thymic hormones stimulate the development and maturation of lymphocytes; and many
hormones affect immune function. The thymus secretes thymic hormones, and cytokines
affect cells throughout the body.

Conversely, the nervous system can apparently adjust the sensitivity of the immune response:

 The PNS innervates dendritic cells in the lymph nodes, spleen, skin, and other antigen-
presenting cells. The nerve endings release neurotransmitters that heighten local immune
responses. For this reason, some skin conditions, such as psoriasis, worsen when a person is
under stress.
 Neuroglia in the CNS produce cytokines that promote an immune response.
 A sudden decline in immune function can occur after even a brief period of emotional
distress.
 28. Identify the role of the lymphatic system for all body systems. 


 Answer: The lymphatic system provides defenses against infection; performs immune

surveillance to eliminate cancer cells; and returns tissue fluid to the circulation.
1. 22-5 In cell-mediated adaptive immunity, presented antigens activate T
cells, which respond by producing cytotoxic and helper T cells
29. Antigen presentation occurs when an antigen–glycoprotein combination appears in
the plasma membrane of an antigen-presenting cell (typically of a macrophage or
dendritic cell). T cells sensitive to this combination are activated if they contact the
membrane of the antigen-presenting cell.
30. All body cells have plasma membrane glycoproteins. The genes controlling their
synthesis make up a chromosomal region called the major histocompatibility
complex (MHC). The membrane glycoproteins are called MHC proteins. APCs
(antigen-presenting cells) are involved in antigen stimulation.
31. Lymphocytes are not activated by free antigens, but respond instead to an antigen
bound to either a class I or a class II MHC protein in a process called antigen
recognition. (Figure 22–18)
32. Class I MHC proteins are in all nucleated body cells. class II MHC proteins are only in
antigen-presenting cells (APCs) and lymphocytes.
33. Whether a T cell responds to antigens held in class I or class II MHC proteins depends
on the structure of the T cell plasma membrane. T cell plasma membranes contain

53
 proteins called CD (cluster of differentiation) markers. CD3 markers are present on
all T cells. CD8 markers are on cytotoxic and regulatory T cells. CD4 markers are on
all helper T cells.
34. One type of CD8 cell responds quickly to a class I MHC–bound antigen, giving rise to
large numbers of cytotoxic T cells and memory T cells. The other type of CD8 cell
responds more slowly, giving rise to small numbers of regulatory T cells.
35. Cytotoxic T cells seek out and destroy abnormal and infected cells, using three
different methods, including the secretion of lymphotoxin. (Figure 22–19)
36. Cell-mediated immunity (cellular immunity) results from the activation of CD8
cells by antigens bound to class I MHCs. When activated, most of these T cells divide
to generate cytotoxic T cells and memory T cells, which remain in reserve to guard
against future such attacks. Regulatory T cells moderate the responses of other T cells
and of B cells. (Figures 22–19,  22–22)
37. Helper T cells, or CD4 cells, respond to antigens presented by class II MHC proteins.
When activated, helper T cells secrete cytokines that aid in coordinating adaptive and
innate defenses and also regulate cell-mediated and antibody- mediated
immunity. (Figures  22–20, Spotlight Figure 22–21)
38. Cytokines are chemical messengers coordinated by the immune
system. Interleukins increase T cell sensitivity to antigens exposed on macrophage
membranes; stimulate B cell activity, plasma cell formation, and antibody production;
enhance innate defenses; and moderate the immune response. (Spotlight Figure 22–
21)
39. Interferons (IFNs) slow the spread of a virus by making the synthesizing cell and its
neighbors resistant to viral infections. (Spotlight Figure 22–21)
40. Tumor necrosis factors (TNFs) slow tumor growth and kill tumor cells, and act as
pyrogens. (Spotlight Figure 22–21)
41. Several cytokines adjust the activities of phagocytes to coordinate innate and adaptive
defenses. (Spotlight Figure 22–21)
42. Colony-stimulating factors (CSFs) are factors produced by active T cells, cells of the
monocyte–macrophage group, endothelial cells, and fibroblasts. (Spotlight Figure 22–
21)

1. 22-6 In antibody-mediated adaptive immunity, sensitized B cells

respond to antigens by producing specific antibodies
43. B cells become sensitized when antibody molecules in their plasma membranes bind
antigens. The antigens are then displayed on the class II MHC proteins of the B cells,
which become activated by helper T cells activated by the same antigen. (Figure  22–
23)
44. An active B cell may differentiate into a plasma cell or produce daughter cells
that differentiate into plasma cells and memory B cells. Antibodies are produced by
plasma cells. (Figure  22–23)
45. A Y-shaped antibody molecule consists of two parallel pairs of polypeptide chains
containing constant and variable segments. (Figure 22–24)
46. The five classes of antibodies (immunoglobulins, Ig) in body fluids are (1) IgG,
responsible for resistance against many viruses, bacteria, and bacterial toxins; (2) IgE,
which releases chemicals that accelerate local inflammation; (3) IgD, located on the

54
 surfaces of B cells; (4) IgM, the first type of antibody secreted after an antigen arrives;
and (5) IgA, found in glandular secretions. (Table 22–1)
47. When antibody molecules bind to an antigen, they form an antigen–antibody
complex. Effects that appear after binding include neutralization (antibody binding
that prevents viruses or bacterial toxins from binding to body
cells); precipitation (formation of an insoluble immune complex)
and agglutination (formation of large complexes); opsonization (coating of pathogens
with antibodies and complement proteins to enhance phagocytosis); stimulation of
inflammation; and prevention of bacterial or viral adhesion. (Figure 22–24)
48. In humoral immunity, the antibodies first produced by plasma cells are the agents of
the primary response. The maximum antibody level appears during the secondary
response to antigen exposure. (Figure 22–25)
49. The initial steps in the immune responses to viral and bacterial infections
differ. (Figures  22–26 to 22–28; Table 22–2)

1. 22-7 Immunocompetence enables a normal immune response;

abnormal responses result in immune disorders
50. Immunocompetence is the ability to produce an immune response after exposure to an
antigen. A developing fetus acquires passive immunity from antibodies in the maternal
bloodstream. After delivery, the infant begins developing active immunity following
exposure to environmental antigens.
51. During periods of stress, interleukin-1 released by active macrophages triggers the
release of ACTH by the anterior lobe of the pituitary gland. Glucocorticoids produced
by the adrenal cortex moderate the immune response, but their long-term secretion can
lower a person’s resistance to disease.
52. Hypersensitivities (allergies) are inappropriate or excessive immune responses
to allergens (antigens that trigger allergic reactions). The four types of allergies
are immediate hypersensitivity (type I), cytotoxic reactions (type II), immune complex
disorders (type III), and delayed hypersensitivity (type IV).
53. In anaphylaxis, a circulating allergen affects mast cells throughout the
body. (Figure 22–29)
54. Autoimmune disorders develop when the immune response inappropriately targets
normal body cells and tissues.

In an immunodeficiency disease, either the immune system does not develop normally or
the immune response is blocked.

consists
The lymphatic system involves of a meandering network of lymphatic vessels. Cancer cells that
break free from the primary tumor can metastasize by the lymph system.

adenitis:
Inflammation of the adenoid (pharyngeal tonsil).

allograft:

55
 Transplant between compatible recipient and donor of the same species.

anamnestic response:
An immune response that is initiated by memory cells.

autograft:
A transplant of tissue that is taken from the same person.

Burkitt lymphoma:
A malignant cancer of B lymphocytes.

chronic fatigue syndrome:

A complicated disorder most often characterized by extreme fatigue that does not improve
with rest, and which may worsen with physical activity.

congenital thymic aplasia:

Congenital (present at birth) absence of the thymus and parathyroid glands and a deficiency
of immunity.

Coombs test:
A medical test to detect antibodies or complement in the blood.

dermatomyositis:
An autoimmune disease characterized by inflammation of the skin and muscles.

eczema:
A genetic inflammatory skin disorder, often with crusts, papules, and leaky eruptions.

Hodgkin lymphoma:
A malignant lymphoma affecting lymph nodes and lymph organs.

host versus graft disease:

A pathological condition in which cells from the transplanted tissue of a donor initiate an
immune response, attacking the cells and tissue of the recipient.

hybridoma:
A tissue culture composed of cancer cells fused to lymphocytes to mass produce a specific
antibody.

56
 immunology:
Branch of biomedicine concerned with the structure and function of the immune system.

infectious mononucleosis:
An acute disease caused by the Epstein–Barr virus, producing fever, swelling of the lymph
nodes, sore throat, and increased lymphocytes in the bloodstream.

latex allergy:
Hypersensitivity to products made of the sap of the rubber plant.

polymyositis:
An autoimmune disease characterized by inflammation and atrophy of muscles.

sentinel node:
The first lymph node to receive drainage from a tumor. It is used to determine if there is
lymphatic metastasis in some types of cancer.

splenomegaly:
Enlargement of the spleen.

systemic lupus erythematosus (SLE):

An autoimmune disease in which a person’s immune system attacks and injures its own
organs and tissues in virtually every system of the body.

xenograft:
A transplant that is made between two different species.

57