Physiology: IMMUNITY

P H Y S I O L O G Y
Dra. Maria Verena Remudaro• April 2020
A.Y. 2019-2020 • 2nd Semester (Midterms)
Transcribers: Ce-ing, Chapasen, Co, Colingey

OUTLINE B. TYPES OF IMMUNITY

I. RESISTANCE OF THE BODY TO
INFECTION: IMMUNITY
A. IMMUNITY
B. TYPES OF IMMUNITY
a. Innate Immunity
b. Acquired Immunity
i. Types of acquired immunity
C. LYMPHOCYTES ARE RESPONSIBLE FOR
ACQUIRED IMMUNITY
D. PREROCESSING OF T LYMPHOCYTES
E. PREPROCESSING OF B LYMPHOCYTES
F. ROLE OF LYMPHOCYTE CLONES
G. ORIGIN OF THE MANY CLONES
H. MECHANISM FOR ACTIVATING A CLONE
a. Role of Macrophages in the
activation process
b. Role of the T Cells in Activation of
the B Lymphocytes
I. HUMORAL IMMUNITY AND THE
ANTIBODIES
a. Formation of Antibodies by Plasma
Cells
b. Formation of “Memory” Cells
J. NATURE OF ANTIBODIES
K. SPECIFICITY OF ANTIBODIES
L. GENERAL CLASSES OF ANTIBODIES
M. MECHANISM OF ACTION OF
ANTIBODIES
N. SPECIAL ATTRIBUTES OF THE T
LYMPHOCYTES
O. TYPES OF T LYMPHOCYTES
a. T Helper
b. Cytotoxic
c. Suppressor
P. TOLERANCE OF THE ACQUIRED
IMMUNITY SYSTEM
Q. IMMUNIZATION BY INJECTION OF
ANTIGENS
R. SUMMARY
a. Innate immunity
 Also called natural or native immunity.
 Result from the general process of the body
when exposed to invading agents.
 Mediates the initial and immediate protection
against infection (provide early defense).
 Always present in healthy individuals.
 Enhances adaptive immune response against
the infectious agents
i. Mechanisms that provide initial
defence against infection
 Prevent infections (through the body’s
epithelial barriers).
 Destruction of swallowed organisms by
acid secretions of the stomach and
digestive enzymes (acid secretions
destroy ingested bacteria).
 Resistance of the skin to invasion by
organisms
 Eliminate microbes
 Phagocytosis of bacteria and other
invaders by WBC
 Presence in the blood of certain chemical
compounds that attach to the foreign
organisms or toxins and destroy them:
 Lysosomes
 Basic polypeptide
 Complement complex
 Natural killer lymphocytes

II. ALLERGY AND HYPERSENSITIVITY

A. TYPES OF HYPERSENSITIVITY
B. IMMEDIATE HYPERSENSITIVITY
REACTIONS

I. RESISTANCE OF THE BODY TO INFECTION:

IMMUNITY

A. IMMUNITY

 Ability of the human body to resist almost all types Figure 1. Innate Immunity
of organisms or toxins that tends to damage the
tissues and organs.
PHYSIOLOGY Resistance of the body to Infection: II Immunity and Allergy
b. Acquired (adaptive) immunity
 Developed powerful specific immunity against
individual invading agents.
 Does not develop until after the body is first
attacked by a bacterium, virus, or toxin, often
requiring weeks or months to develop the
immunity
 Also called specific acquired immunity
 Develops more slowly (it takes weeks to
months)
 Mediates a more effective and specific
defense against infections
 Product of the body’s lymphocytes
 Located on the lymph nodes and special
lymphoid tissues (tonsils, adenoids,
submucosal areas of the GIT, spleen, thymus,
bone marrow)
 Distributed advantageously in the body to
intercept invading organisms and toxins before
they can spread too widely.
C.
Figure 2.
i. Mediated by lymphocytes
 B lymphocytes produce antibodies which
block infections and eliminate microbes
 T lymphocytes eradicate intracellular
microbes
 Caused by a special immune system that
forms antibodies and/or activated
lymphocytes that attack and destroy the
specific invading organism or toxin.
ii. Basic Types of Acquired Immunity
 Humoral (B cell) immunity
 The body develops circulating antibodies
which are globulin molecules in the blood
plasma that are capable of attacking the
invading agent.
 B lymphocytes produce the antibodies.
 Cell mediated (T cell) immunity
 Formation of large number of activated T
lymphocytes that are specifically crafted in
the lymph nodes to destroy the foreign agent
 Activated lymphocytes are T lymphocytes
 both the antibodies and the activated
lymphocytes are formed in the lymphoid
tissues of the body.
 Both types of acquired immunity develop after
invasion by a foreign organism or toxin
(antigens).
 Antigens- Proteins or large polysaccharides
with regularly recurring molecular groups
(epitopes) on the surface of these large
molecules (This explains why proteins and large
polysaccharides are almost always antigenic,
because both of these have this stereochemical
characteristic).
 For a substance to be antigenic, it usually must
have a high molecular weight, 8000 or greater.
LYMPHOCYTES ARE RESPONSIBLE FOR
ACQUIRED IMMUNITY
 The lymphocytes are located most extensively in
the lymph nodes but they are also found
especial lymphoid tissues such as the spleen,
submucosal areas of the gastrointestinal tract,
thymus, and bone marrow.
 The lymphoid tissue is distributed
advantageously in the body to intercept
invading organisms or toxins before they can
spread widely.
1 2
Figure 3
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a. Major populations of lymphocytes F. ROLE OF LYMPHOCYTE CLONES

i. T lymphocytes  Each of these preformed lymphocytes is capable

 Responsible for forming the activated of forming only one type of antibody or one type
lymphocytes that provide “cell-mediated” of T cell with a single type of specificity, and only
immunity. the specific type of antigen can activate it.
ii. B lymphocytes  Once the specific lymphocyte is activated by its
 Responsible for forming antibodies that antigen, it reproduces wildly, forming
provide “humoral” immunity. tremendous numbers of duplicate lymphocytes.
 Almost all of the formed lymphocytes eventually
end in the lymphoid tissue. But before T and B
Lymphocytes end up in the lymphoid tissue, they
needed to be preprocessed.

D. PREPROCESSING OF THE T LYMPHOCYTES

 The thymus gland preprocesses the T

lymphocytes. Thus they are called “T”
lymphocytes to designate the role of the thymus.
 It first mixes them with all the specific “self-
antigens” from the body’s own tissues. It selects
and releases only those cells that are non-
reactive against the body’s own antigen and
reacts against antigen from an outside source.
 In the preprocessing of lymphocytes, the
lymphocytes recognize a person’s own tissue
and all of the clones that damages the body’s
own tissues are destroyed. This is called
TOLERANCE
 Failure of tolerance mechanism causes
Autoimmune Disease.
 Once thymic lymphocyte develops specific
reactivity against one antigen. Then the next
lymphocyte develops specificity against another
antigen. These different types of preprocessed T
lymphocytes now leave the thymus and spread
by way of the blood throughout the body to
lodge in lymphoid tissue everywhere.

E. PREPROCESSING OF THE B LYMPHOCYTES Figure 4. An antigen activates only lymphocytes

 B lymphocytes that are destined to form
antibodies—are preprocessed in the liver during
mid–fetal life and in the bone marrow in late fetal
life and after birth.
 Once presented with specific antigen during
preprocessing period the B lymphocytes actively
secretes antibodies which are capable of
combining with and destroying antigenic
substance. They show greater diversity by
forming millions of antibodies with different
specific reactivates.
 After preprocessing, the B lymphocytes migrate
to lymphoid tissue throughout the body and
remain dormant, where they lodge near but
slightly removed from the T-lymphocyte areas.
that have cell surface receptors that are
complementary and recognize a specific antigen.
Millions of different clones of lymphocytes exist.
When the lymphocyte clone is activated by its
antigen, it reproduces to form large numbers of
duplicate lymphocytes, which can secrete
antibodies.
 All of the lymphocytes that are capable of
forming one specific antibody or T cell are called
a clone of lymphocytes. That is, the lymphocytes
in each clone are alike and are derived originally
from one or a few early lymphocytes of its
specific types.
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 T lymphocytes and B lymphocytes react highly
specifically against specific antigen that initiated
their development forming clone of lymphocytes
 They are stored in the lymphoid tissue and
lymph nodes
 Once this specific lymphocyte is activated by its
antigen, it reproduces forming duplicate
lymphocytes
 Acquired immunity is the product of the body’s
lymphocytes.
G. ORIGIN OF THE MANY CLONES OF
LYMPHOCYTES
 The whole gene for forming each type of T cell or
B cell is never present in the original stem cells
from which the functional immune cells are
formed. Instead, there are only “gene segments”—
actually, hundreds of such segments—but not
whole genes.
 During preprocessing of the respective T- and B-
cell lymphocytes, these gene segments become
mixed with one another in random combinations,
in this way finally forming whole genes.
 For each functional T or B lymphocyte that is
finally formed, the gene structure codes for only a
single antigen specificity. These mature cells then
become the highly specific T and B cells that
spread to and populate the lymphoid tissue.
H. MECHANISM FOR ACTIVATING A CLONE OF
LYMPHOCYTES
 In the case of the B lymphocytes, each of these
has on the surface of its cell membrane about
100,000 antibody molecules that will react highly
specifically with only one specific type of antigen.
Therefore, when the appropriate antigen comes
along, it immediately attaches to the antibody in
the cell membrane; this leads to the activation
process.
 In the case of the T lymphocytes, molecules
similar to antibodies, called surface receptor
proteins (or T-cell markers), are on the surface of
the T-cell membrane, and these are also highly
specific for one specified activating antigen. An
antigen therefore stimulates only those cells that
have complementary receptors for the antigen and
are already committed to respond to it.
a. Role of Macrophages in the activation
process
 Most invading organisms are first phagocytized
and partially digested by the macrophages, and
the antigenic products are liberated into the
macrophage cytosol.
 The macrophages then pass these antigens by
cell-to-cell contact directly to the lymphocytes,
thus leading to activation of the specified
lymphocytic clones.
 Interleukin-1 – secrete by macrophage that
promotes still further growth and reproduction of
the specific lymphocytes.
b. Role of the T Cells in Activation of the B
Lymphocytes.
 Some of the T cells that are formed, called helper
cells, secrete specific substances (collectively
called lymphokines) that activate the specific B
lymphocytes. Indeed, without the aid of these
helper T cells, the quantity of antibodies formed by
the B lymphocytes is usually slight
I.HUMORAL IMMUNITY AND THE
ANTIBODIES
a. Formation of Antibodies by Plasma Cells
 Before exposure to a specific antigen, the clones
of B lymphocytes remain dormant in the lymphoid
tissue. Upon entry of a foreign antigen,
macrophages in the lymphoid tissue phagocytize
the antigen and then present it to adjacent B
lymphocytes.
 In addition, the antigen is presented to T cells at
the same time, and activated helper T cells are
formed.
 These helper cells also contribute to extreme
activation of the B lymphocytes,
 The B lymphocytes specific for the antigen
immediately enlarge and take on the appearance
of lymphoblasts. Some of the lymphoblasts further
differentiate to form plasmablasts, which are
precursors of plasma cells. In the plasmablasts,
the cytoplasm expands and the rough
endoplasmic reticulum vastly proliferates. The
plasmablasts then begin to divide at a rate of
about once every 10 hours for about nine
divisions.
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b. Formation of “Memory” Cells enhances the
antibody response to subsequent antigen
exposure
 The B-cell population of the specifically activated
clone becomes greatly enhanced, and the new B
lymphocytes are added to the original lymphocytes
of the same clone.
 They remain dormant until activated once again by
a new quantity of the same antigen. These
lymphocyte are called memory cells.
 Subsequent exposure to the same antigen will
cause a much more rapid and much more potent
antibody response this second time around,
because there are many more memory cells than
there were original B lymphocytes of the specific
clone.
Figure 5. The primary response for forming antibodies
that occurs on first exposure to a specific antigen and
the secondary response that occurs after second
exposure to the same antigen. Note the 1-week delay
in the appearance of the primary response, its weak
potency, and its short life. The secondary response, by
contrast, begins rapidly after exposure to the antigen, is
far more potent, and forms antibodies for many months
rather for only a few weeks. The increased potency and
duration of the secondary response explain why
immunization is usually accomplished byinjecting
antigen in multiple doses with periods of several weeks
or several months between injections.
 Upon the first exposure with antigen, the body
produces a primary
 Response of forming antibodies to neutralize
antigen.
 Role of Memory Cells – if the same antigen
invades the body, memory cells will become
activated and produce a much more rapid and
more potent antibodies response compared to the
first exposure.
J. NATURE OF ANTIBODIES
 They are gamma globulins called
immunoglobulins.
 Each antibody is specific for a particular antigen.
 Light chain
 Heavy chain
 Each heavy chain is paralleled by light chain’s
end.
 There at least 2 light chains (IgG) and as many
as 10 light chains (IgM) to each immunoglobulin.
 Disulfide bonds hold the chains together.
Figure 6. Structure of the typical AgG antibody,
showing it to be composed of two heavy chains and
two light polypeptide chain. The antigen binds at two
different sites on the variable portions of the chain.
a. Variable Portion
 Different for each specific antibody
 Attaches to a particular type of antigen
b. Constant Portion
 Determines antibody diffusivity in the tissues
 Adherence to specific structure within the
tissues
 Attachment to the complement complex
 Ease of passing through membranes
 Other biological properties
K. SPECIFICITY OF ANTIBODIES
 Each antibody is specific for a particular antigen;
this characteristic is caused by its unique
structural organization of amino acids in the
variable portions of both the light and heavy
chains.
 The amino acid organization has a different
steric shape for each antigen specificity, so
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when an antigen comes in contact with it,
multiple prosthetic groups of the antigen fit as a
mirror image with those of the antibody, thus
allowing rapid and tight bonding between the
antibody and the antigen
 Class switch – causes expression of new
antibodies. Constant region will be changed but
not the variable region. Thus it can still
recognize the antigen
 E.g. Primary exposure to a viral antigen, IgM is
produced initially but will undergo class switch to
IgG on re-exposure to the same virus.
L. GENERAL CLASSES OF ANTIBODIES
Figure 7. General classes of antibodies
M. MECHANISM OF ACTION OF ANTIBODIES
a. Direct attack on the invader by:
i. Agglutination- in which multiple large particles
with antigens on their surfaces, such as bacteria
or red cells, are bound together into a clump.
ii. Precipitation- in which the molecular complex
of soluble antigen (such as tetanus toxin) and
antibody becomes so large that it is rendered
insoluble and precipitates.
iii. Neutralization- in which the antibodies cover
the toxic sites of the antigen agent.
iv. Lysis- in which some potent antibodies are
occasionally capable of directly attacking
membranes of cellular agents and thereby
cause rupture of the agent.
b. Activation of the Complement System that
has multiple means of its own for
destroying the invaders.
 Complement system is a collective term that
describes a system of about 20 proteins present
normally in the blood
 Many of which are enzyme precursors (C1 to
C9, B, D)
 These enzyme precursors are normally
inactivated by the classic pathway
 Initiated in turn by an antigen-antibody reaction.
Figure 8
 Classical Pathway. The classical pathway is
initiated by an antigen-antibody reaction. That is,
when an antibody binds with an antigen, a specific
reactive site on the “constant” portion of the
antibody becomes uncovered, or “activated,” and
this in turn binds directly with the C1 molecule of
the complement system, setting into motion a
“cascade” of sequential reactions, beginning with
activation of the proenzyme C1. The C1 enzymes
that are formed then activate successively
increasing quantities of enzymes in the later
stages of the system so that from a small
beginning, an extremely large “amplified” reaction
occurs. Multiple end products are formed, as
shown to the right in the figure, and several of
these cause important effects that help to prevent
damage to the body’s tissues caused by the
invading organism or toxin. Among the more
important effects are the following:
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i. Opsonization and phagocytosis
 C3b, strongly activates phagocytosis by both
neutrophils and macrophages, causing these
cells to engulf the bacteria to which the antigen-
antibody complexes are attached.
ii. Lysis
 Has a direct effect of rupturing the cell
membranes of bacteria or other invading
organisms.
iii. Agglutination
 The complement products also change the
surfaces of the invading organisms, causing them
to adhere to one another, thus promoting
agglutination.
iv. Neutralization of viruses
 The complement enzymes and other complement
products can attack the structures of some
viruses and thereby render them nonvirulent.
v. Chemotaxis
 Fragment C5a initiates chemotaxis of neutrophils
and macrophages, thus causing large numbers
of these phagocytes to migrate into the tissue
area adjacent to the antigenic agent.
vi. Activation of mast cells and basophils
 Fragments C3a, C4a, and C5a activate mast
cells and basophils, causing them to release
histamine, heparin, and several other
substances into the local fluids. These
substances in turn cause increased local blood
flow, increased leakage of fluid and plasma
protein into the tissue, and other local tissue
reactions that help inactivate or immobilize the
antigenic agent.
vii. Inflammatory effects
 caused by activation of the mast cells and
basophils, several other complement products
contribute to local inflammation. These products
cause (1) the already increased blood flow to
increase still further, (2) the capillary leakage of
proteins to be increased, and (3) the interstitial
fluid proteins to coagulate in the tissue spaces,
thus preventing movement of the invading
organism through the tissues.
N. SPECIAL ATTRIBUTES OF THE T-LYPMPHOCYTE
SYTEM- ACTIVATED T CELLS AND CELL-
MEDIATED IMMUNITY
a. T Lymphocytes
 Respond to antigens only when they are
bound to specific molecules called MHC
proteins on the surface of antigen-presenting
cells
 Macrophages
 B lymphocytes
 Dendritic cells - most potent of the
antigen-presenting cells, located
throughout the body, and their only
known function is to present antigens to
T cells
 T lymphocyte shave T cell receptor in its
surface for the binding of antigen.
Figure 9. T Lymphocyte System
 Upon exposure to the proper antigen, as
presented by adjacent macrophages, the T
lymphocytes of a specific lymphocyte clone
proliferate and release large numbers of
activated, specifically reacting T cells in ways that
parallel antibody release by activated B cells. The
principal difference is that instead of releasing
antibodies, whole activated T cells are formed
and released into the lymph. These T cells then
pass into the circulation and are distributed
throughout the body, passing through the
capillary walls into the tissue spaces, back into
the lymph and blood once again, and circulating
again and again throughout the body, sometimes
lasting for months or even years.
 Also, T-lymphocyte memory cells are formed in
the way that B memory cells are formed in the
antibody system. That is, when a clone of T
lymphocyte is activated by an antigen, many of
the newly formed lymphocytes are preserved in
the lymphoid tissue to become additional T
lymphocytes of that specific clone; in fact, these
memory cells even spread throughout the
lymphoid tissue of the entire body.
 Therefore, on subsequent exposure to the same
antigen anywhere in the body, release of
activated T cells occur far more rapidly and much
more powerfully than during the first exposure.
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 Although B lymphocytes recognize intact
antigens, T lymphocytes respond to antigens only
when they are bound to specific molecules called
MHC proteins on the surface of antigen-
presenting cells in the lymphoid tissues.
O. TYPES OF T LYMPHOCYTES
Figure 10. Activation of T cells requires interaction
of T-cell receptors with an antigen that sis
transported to the surface of the antigen-presenting
cell by a major histocompatibility complex (MHC)
protein. Cell-to-cell adhesion proteins enable the T
cell to bind to the antigen-presenting cell long
enough to become activated.
 The three major types of antigen-presenting
cells are
o Macrophages
o B lyphocytes
o Dendritic cells- most potent, are located
throughout the body, and their only
known function is to present antigens to
T cells.
 The MHC proteins are encoded by a large group
of genes called major histocompatibility complex
(MHC).
Figure 11
 MHC proteins bind peptide fragments of antigen
proteins that are degraded inside antigen-
presenting cells and then transport them to the
cell surface.
 Two types of MHC proteins: (1) MHC I proteins,
which present antigens to cytotoxic T cells, and
(2) MHC II proteins, which present antigens to T
helper cells.
a. T helper cells
 Help B lymphocytes to make the most
effective antibodies and help macrophages to
kill ingested microbes.
 Serve as major regulator of all immune
response.
 Form a series of protein mediators called
lymphokines (Il-2,3,4,5,6, IFN, GM-CCSF)
 It is the helper T cells that are inactivated or
destroyed by the acquired immunodeficiency
syndrome (AIDS) virus, which leaves the body
almost totally unprotected against infectious
disease.
i. Stimulation of Growth and
proliferation of cytotoxic T cells and
suppressor T cells (II-2)
 The lymphokine interleukin-2 has an
especially strong stimulatory effect in
causing growth and proliferation of both
cytotoxic and suppressor T cells.
ii. Stimulation of B cell growth and
differentiation to form plasma cells
and antibodies
 Interleukins 4, 5, and 6 have such
potent effects on the B cells that they
have been called B-cell stimulating
factors or B-cell growth factors.
iii. Activation of the macrophage
system
iv. Feedback Stimulatory effect on the
T helper cell
 Interleukin-2, have a direct positive
feedback effect in stimulating activation
of the helper T cells.
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b. Cytotoxic (Cytolytic) T Lymphocytes
(CTLs)
 Kill infected host cells and thus serve to
eliminate reservoir of infection.
 Cytotoxic cells also play an important role in
destroying cancer cells, heart transplant cells,
or other types of cells that are foreign to the
person’s own body.
 Direct attack cells.
Figure 12. Direct destruction of an invading cell
by sensitized lymphocytes (cytotoxic T cells).
c. Suppressor T cell
Q. IMMUNIZATION BY INJECTION OF ANTIGENS
 Small population of lymphocytes which control
immune responses and prevent inappropriate
reactions that might damage the body’s own
tissues.
 Capable of suppressing the function of both
cytotoxic and T helper cells.
 Suppressor T-cell system plays an important
role in limiting the ability of the immune system
to attack a person’s own body tissues, called
immune tolerance.
P. TOLERANCE OF THE ACQUIRED IMMUNITY
SYSTEM TO ONE’S OWN TISSUES-TOLE OF
PREPOROCESSING IN THE THYMUS AND
BONE MARROW
a. Most Tolerance Results from Clone
Selection During Preprocessing
 During the preprocessing of lymphocytes in
the thymus and bone marrow, all or most of
those clones of lymphocytes that are
specific to damage the body’s own tissues
are self-destroyed because of their continual
exposure to the body’s antigens.
b. Failure of the Tolerance Mechanism
Causes Auto Immune Diseases
 Lose of immune tolerance, occurs after
destruction of some of the body’s own
tissues, which releases considerable
quantities of “self-antigens” that circulate in
the body and presumably cause acquired
immunity in the form of either activated T
cells or antibodies.
 Several specific diseases that result from
autoimmunity
i. Rheumatic fever
 Exposure to a specific type of
streptococcal toxin that has an
epitope in its molecular structure
similar to the structure of some of
the body’s own self-antigens;
ii. Glomerulonephritis
iii. Myasthenia Gravis
 Immunity develops against the
acetylcholine receptor proteins of
the neuromuscular junction,
causing paralysis; and
iv. Lupus Erythematosus
 Person becomes immunized
against many different body
tissues at the same time, a
disease that causes extensive
damage and often rapid death.
 A person can be immunized by injecting dead
organisms that are no longer capable of causing
disease but that still have some of their chemical
antigens. This type of immunization is used to
protect against typhoid fever, whooping cough,
diphtheria, and many other types of bacterial
diseases
 Immunity can be achieved against toxins that
have been treated with chemicals so that their
toxic nature has been destroyed even though
their antigens for causing immunity are still intact
(ex. tetanus, botulism).
 Person can be immunized by being infected with
live organisms that have been “attenuated.” (ex.
smallpox, yellow fever, poliomyelitis, measles,
and many other viral diseases).
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a. Types of Adaptive Immunity
i. Active immunity
 The person’s own body develops either
antibodies or activated T lymphocytes in
response to invasion of the body by a
foreign antigen.
ii. Natural immunity
iii. Vaccine induced immunity (live
attenuated, inactivated, subunit)
Figure 13.
b. Passive Immunity
 Transfusion of antibodies or T lymphocytes to
confer raped protection but for a short period
of time.
 Activated T cells last for a few weeks if
transfused from another person but only for a
few hours to a few days if transfused from an
animal.
 Maternal IgG
 Introduction of antibodies by injection.
R. SUMMARY
 If a pathogen invades the body, the first response
is our innate immunity it can be through the
digestive enzymes or tissue macrophages in the
first line defense that later on, can activate the
neutrophils and more macrophages going to the
area of infection and also stimulate/activate the
Natural Killer cells and dendritic cells.
 Macrophages together with dendritic cells can
ingest fragments of antigen to become antigen
presenting cells (APC) and presents antigen to T
lymphocytes.
 B and T lymphocytes will be the adaptive immunity
which is more potent and more effective immunity.
 T lymphocytes will proliferate and kill the pathogen
while the B lymphocytes will form the antibodies.
 Re-exposure to the same antigen will activate
memory cells to produce specific antibodies against
the antigen.
Figure 14.
II. ALLERGY AND HYPERSENSITIVITY
 Important undesirable side effect of immunity.
 Classified according to the principal immunologic
mechanism that is responsible for tissue injury and
disease.
 Delayed-reaction allergy is caused by activated T
cells and not by antibodies.
A. TYPES OF HYPERSENSITIVITY REACTIONS
 Types I through III are mediated by antibodies,
while type IV is mediated by T cell lymphocytes.
i. Type I Hypersensitivities
 Involve IgE antibodies that initially sensitize an
individual to an allergen and provoke a quick
inflammatory response upon subsequent
exposure.
 Allergies and hay fever are both type I.
ii. Type II Hypersensitivities
 Involve the binding of IgG and IgM antibodies to
antigens on cell surfaces.
 This induces a cascade of events that leads to
cell death. Hemolytic transfusion reactions and
hemolytic disease of newborns are type II
reactions.
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iii. Type III Hypersensitivities d. Hay fever

 Result from the formation of antigen-antibody
complexes that settle on tissues and organs.
 In an attempt to remove these complexes,
underlying tissue is also damaged. Serum
sickness and rheumatoid arthritis are examples
of type III reactions.
iv. Type IV Hypersensitivities
 Are regulated by T cells and are delayed
reactions to antigens associated with cells.
 Tuberculin reactions, chronic asthma, and
contact dermatitis are examples of type IV
reactions.
 The allergen-reagin reaction occurs in the
nose.
e. Asthma
 The allergen-allergin occurs in the
bronchioles of the lungs.
 Slow-reacting substance of anaphylaxis
causes spasm of the bronchiolar smooth
muscle. Consequently, the person has
difficulty breathing until the reactive products
of the allergic reaction have been removed.
References:

B. IMMEDIATE HYPERSENSITIVITY REACTIONS Guyton and Hall Textbook of Medical Physiology,

12th ed.
a. Atopic Allergies
Powerpoint presentation of Dr. Remudaro
 Caused by a non-ordinary response of the
immune response characterized by the
presence of large quantities of IgE
antibodies in the blood
 The allergic tendency is genetically passed
from parent to child and is characterized by
the presence of large quantities of IgE
antibodies in the blood. These antibodies
are called reagins or sensitizing antibodies
 When an allergen enters the body, an
allergen-reagin reaction takes place and a
subsequent allergic reaction occurs.
 Allergen – an antigen that reacts specifically
with a specific type of IgE reagin antibody.

b. Anaphylaxis
 A widespread allergic reaction occurring
throught the vascular system and closely
associated tissues
 Histamine is released causing widespread
vasodilation

c. Urticaria
 Results from antigen specific skin areas and
causing localized anaphylactoid reaction
 Histamine released locally causes (1)
vasodilation that induces an immediate red
flare and (2) increased local permeability of
the capillaries that leads to local
circumscribed areas of swelling of the skin
(hives).

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