Week 1 Study Guide

What are the ways that the body protects us?

 The Immune System

o WBC

 KEY PLAYERS- look for foreign invaders (microbes)

 B cells, T Cells and Natural killer cells

o Antibodies

 Fight microbes and toxins – recognizing antigens for

destruction

o Complement System

 Plasma Proteins (liver)

 Recruit phagocytes

 Activate mast cells

 Destroy pathogens

 Activation of C3 and C5 proteins by:

 Opsonins

 Chemokines

 C5b- C9 membrane attack complexes

 Marks pathogens for destruction

o Lymphatic System

 Delicate tubes:

 Manage the fluid levels

  React to bacteria

 Deal with cancer cells

 Cell products disease and disorders

 Absorb some fat from diet

 Lymph nodes: trap microbes

 Lymph vessels: contains infection fighting WBC

 WBC

o Spleen

 Blood filtering organ – removes microbes

 Destroys old or damaged RBC

 Creates antibodies and lymphocytes

o Bone Marrow

 Spongy tissue inside bones

 Produces RBC for oxygen

 Produces WBC to fight infection

 Produces platelets to help clot

o Thymus

 Filters and monitors blood content

 Produces WBC – T Lymphocytes

What is the difference between innate and immune response? 

Line of Timeline Cells Antigen Examples

 Defense Dependency
Innate – First Immediate Natural Killer Cells, independent Skin, hair,
NonSpecific Response Macrophages, cough, mucous,
(0-96 Neutrophils, dendritic membranes,
hours) cells, mast cells, phagocytes,
basophils, eosinophils granulocytes
Adaptive – Second Long Term T and B Lymphocytes dependent Puss, swelling,
Specific (>96 hours) redness, pain, T
and B
lymphocyte
response

When do you have an innate response?

 The first time interacting with an antigen – activated immediately

(rapid) once a pathogen attacks.

What is the purpose of the inflammation response?

 General Immune Response: Inflammation

o Brings immune cells to the site of infection

 Increasing blood flow to area

o Neutralizes harmful agents

o Is vascular

o removes damaged or necrotic tissue, regenerates

What happens in the vascular stage of inflammation?

 First Phase

 VASODILATION

o Blood flow to the area increases

o Slows blood velocity

 o Red and warm

 CAPILLARY PERMEABILITY

o Chemical Mediators allow exudate to escape into tissues

 Histamine

 Bradykinin

 Leukotrienes

o Increase concentration of blood cells, stops flow, starts clotting

o this causes: Redness, edema, swelling, pain, impaired function.

What happens in the cellular stage of inflammation?

 WBC travel to injured tissue

o Margination and tethering – accumulation and adhesion

(selectin, integrin)

o Transmigration and chemotaxis

 Once recognized: Phagocytosis is activated

o move in to remove microbes or foreign bodies

 neutrophils, eosinophils, macrophages

o opsonization, engulfment, phagosome

1. histamine and prostaglandin is released

2. Capillaries dilate, clotting begins

3. Chemotactic factors attract phagocytic cells

4. Phagocytes consume pathogens and cell debris

What is exudate?
  Following Phagocytosis: EXUDATES is formed

o made up of fluid, proteins, RBCs, leukocytes, cell debris

 Types: serous, fibrinous, purulent (cyst, abcess), hemorrhagic or

sanguinous

How does the body mount a systemic inflammatory response?

1. CRP- binds to pathogen (opsonin) marking it for phagocytosis

2. SAA- increased HDL to macrophages

3. Fibrinogen- Increased erythrocyte sedimentation rate (ESR)

When does a systemic response happen?

 Severe Infection – uncontrolled infection

 Sepsis, septic shock, multiple organ dysfunction syndrome

What do you see when there is a systemic response?

 Fever or hypothermia

 Tachycardia – increased heart rate > 100 BMP

 Tachypnoea – abnormal rapid breathing >20 Respiratory rate

 Leukocytosis >WBC count (infection)

 Increase in circulating plasma proteins

What are the functions of interleukins, tumor necrosis factor, and

interferons? 

 Interleukins (IL):
o Produced by macrophages
o Calls lymphocytes and WBCS into action – immunotherapy
o Induces fever
o Stimulates bone marrow cell production
  Tumor necrosis factor (TNF):
o produced mainly by macrophages and T cells, can cause
cancer cell death; responds to gram negative bacteria, virus
infected cells, cancer cells
 Interferons (INF):
o produced by host cells invaded by viruses or cancer
o signals protein release, slow growth, cell defense
o inhibits cancer proliferation (DNA) and viral binding  
o DOES NOT save cell already infected by virus!

What is the function of the mast cells?

 Most important activator in inflammatory response

o Once activated – moves to injury site

o Phagocyte

o Releases chemical mediators

Mast Cell Secretions:

 histamine release: biochemical mediator
o releases vasoactive amines
o causes vasodilation/ vasoconstriction
o causes increased vascular permeability
o causes bronchoconstriction
o parasympathetic response
 Leukotriene
o Increased vascular permeability
o Smooth muscle contraction
 Bronchoconstriction (parasympathetic)
o Act later/ last longer than histamine in response
 Prostaglandins
o Vascular permeability
o Vasodilation
o Smooth muscle contraction
 Bronchoconstriction (parasympathetic)
o Induces pain
o Causes neutrophil chemotaxins
What is a chemokine?

 Attract specific type of WBC to inflammation site

 neutrophils, eosinophils

What does it mean to be pleiotropic and redundant?

 Pleiotropy: one cell can act on various different cells; many functions 
 Redundant: cytokines that produce similar signals to one another

What do neutrophils, macrophages and dendritic cells do?

 Neutrophils: first responders- arrive within 90 minutes of injury

o Increase acute infection
o Phagocytic- engulf bacteria
o release chemical mediators 
o pus cells
 Macrophages: phagocytosis
o Scavenger cells
o secretion of cytokines - cause inflammation
o aids in wound preparation and remodeling
o antigen-presenting cells- adaptive immunity
o produce cytokines and co stimulators
 active t cells, b cells, innate immune cells
 Dendritic cells: phagocytic cells of innate immune system
o Under epithelial tissue (skin, lungs, nose, gi)
o Capture dead cells, pathogens
o Secrete cytokines
o Migrate to regional lymph nodes
o Antigen-presenting cells: activates helper T cells

What is the difference between acute inflammation and chronic

inflammation?

 Acute inflammation:
o self limiting
o onset to damage healing - SHORT (8-10 days)
 Chronic inflammation:
o Lasts for 2 weeks or longer
 o Dense infiltration of lymphocytes and macrophages
o Low grade, persistent infections, irritants
o Develops if acute response is inadequate

When do you see an abscess and when do you see a granuloma?

 Abcess: localized inflammation with purulent exudate

o Necrotic core with pus, surrounded by neutrophils

o Fibroblasts wall off

 Granuloma: chronic inflammation

o 2-3 mm lesion surrounded by macrophages, resembling

epithelial cells

o Cells clump in a mass, surround pathogen

o Membrane of connective tissue encapsulates and isolates

o Splinter, sutures, TB, syphilis

What are the antigen presenting cells and what function do they serve
in adaptive immunity?

 Macrophages, dendritic cells, B cells

 Activate Helper T cells
 recognize antigens from past exposure and have developed a
memory of the antigen; epitope is processed and recognized, present
to CD4 T helper cells to signal an immune response

When does adaptive immunity start?

 Adaptive immunity starts when the body recognizes an antigen it has
had exposure to in the past - takes several days to mount the full
response.

What is adaptive immunity?

What cells take part in it?

  Cells: helper T-cells(CD4), cytotoxic T-cells (CD8), B-cells

What function do the helper T cells play?

 activate B cells, cytotoxic T cells

 secrete cytokines to activate macrophages and NK cells
 How do they identify antigens and activate the immune system?
o Recognize specific antigen peptide fragments bound to MHC-I

How does the major histocompatibility complex (MHC1 and MHC2)

play a role in adaptive immunity?

 MHC1: Produced by all nucleated cells, platelets

 MHC2: produced by antigen presenting cells- dendritic cells,

macrophages, b cells

How do they interact with T helper cells and cytotoxic T cells?

 MHC1: cytotoxic T cells – recognized by CD8+ cytotoxic t cells -

destroy infected cells by secreting perforin 
 MHC2: helper T cells – epitope processed and presented to CD4+ T
helper cells – signal immune responses

What is an epitope?

 Antigenic determinant (epitope)

o Area of the antigen recognized by immune systems

How do antibodies and antigens bind to each other?

1. Antigen: Foreign Molecule – that reacts with parts of the immune

system

2. Antigenic determinant (epitope)

3. Antigen- binding site (paratope)

4. Antigen fits into binding site of the antibody “key into a lock”
How do antibodies function?

 Binding of antibodies to antigens inactivates antigens by:

o Neutralization – blocks viral binding sites, coats bacteria
o Agglutination of antigen-bearing particles (microbes)
 Phagocytosis- macrophage
o Precipitation of soluble antigens
o Complement fixation (activation of complement)
 Foreign cell leads to: cell lysis

Differentiate between antibody primary response and secondary

response.

 Primary: IgM (10%)

o Initial encounter with antigen – binds to a receptor on a specific

B lymphocyte

o Proliferation to form a clone

o Secreted antibody molecules

 Secondary: IgG (75-80%)

o Most common form

o Can be years later

o Clone of cells identical to ancestral cells

o Subsequent challenge by same antigen

o Crosses placenta

What are the different types of antibodies? 

 IgM- primary
 IgG- most common, crosses placenta
 IgA- secreted from mucus membranes, breast milk
 IgD
  IgE- histamine reactions and allergies, parasite infections, basophils
and mast cells

What role do complement proteins play in innate (inflammatory) and

immune (antibody) reactions?

What are some examples of active and passive immunity?

 Active immunity:
o exposure to antigen (catching a disease)
o immunizations
 Passive immunity:
o maternal antibodies transferred through placenta and breast
milk
o gamma globulin

Why do you need a booster shot with active immunity?

 Takes weeks- months to develop, long lasting

 Adults should receive booster every 10 years

How is HIV diagnosed? What are the different stages? 

1. ELISA/EIA- enzyme immune assays

2. If positive: use WESTERN BLOT ASSAY- to differentiate and confirm
3. PCR (newborns- 18 months) – identifies viral DNA only
 4. Orasure and oraquick rapid HIV-1 antibody test followed by western
blot test
5. If HIV positive, monitor CD4 count, viral load
1. CD4 count: below 200 cells/ul OR an AIDS defining condition

What are the most common opportunistic infections seen with HIV?

 Gastrointestinal
 Pulmonary ***
o Pneumonia
o Tuberculosis: globally most common cause of death
 Malignancy
o Kaposi sarcoma
o NH lymphoma
o Cervical and anal cancer
 Gynecologic
o Vaginitis
o Dysplasia
 Sexually transmitted co infections

What do the HIV/AIDS therapies accomplish?

 Slows down progression of the disease by targeting cell cycle at

different stages; uses at least 3 classes of antiretroviral drugs

Class Questions

Eosinophils are predominant in ____ and ____.

A. Allergic reactions and autoimmune response

B. Chronic inflammation and cell mediated hypersensitivity

C. Allergic reactions and parasitic infections

D. Chronic inflammation and antibody response

Natural killer cells are specialized lymphocytes that are the major
parts of which of the following types of immunity?
 A. Cell-mediated immunity

B. Adaptive immunity

C. Innate immunity

Humoral (antibody) immunity Innate immunity utilizes cells that

produce cytokines, which mediate immune cell actions. How are the
actions of cytokines described? (Select all)

A. Rapid and self limiting

B. Pleotrophic and redundant

C. Cell specific and targeted

D. Dendritic and morphologic

E. Cell specific and morphologic

Which leukocytes participate in the inflammatory response?

A. Eosinophils

B. Monocytes

C. Neutrophils

D. All of the above

E. A and C

Which causes the redness (erythema) associated with the

inflammatory process?

A. Prostaglandins

B. Histamine

C. Macrophages

D. All of the above

 E. A and B

A pathology report notes that there is an abscess in your patient’s

lung. The patient asks for an explanation of this finding. How would
you describe this?

A. A small area of scar tissue containing new blood vessels and

fibroblasts

B. A small area containing pus made up of apoptotic neutrophils walled

off by fibroblasts

C. An accumulation of macrophages and fibroblasts

D. An accumulation of macrophages and connective tissue

encapsulating an persistent infection

The cardinal signs of inflammation are swelling, redness, pain, and

heat. What is the 5th cardinal sign?

a. Sepsis

b. Rubor

c. Fever

d. Loss of function

A man initially had symptoms of a fever, productive cough, and

bloody sputum. Later, he had trouble breathing, and the doctor said
his lungs were “consolidated”. He recovered and his fever went
down; he thought he was cured. Three years later, an x-ray showed
nodules in his lungs. Which inflammatory events occurred in this
case?

A. Granuloma

Which immune cell creates antibodies in response to antigens?

A. Cytotoxic T lymphocytes

B. Helper T lymphocytes
 C. Cytokines

D. B lymphocytes

One of the self-regulatory actions of the immune system is to identify

self-antigens. What is this ability called?

B. Antigen specificity

C. Autoantibody formation

D. Tolerance

E. Antigen diversity

True or false? A vaccination is an example of passive immunity. False

A woman was bitten by a rattlesnake last summer; she received

antiserum against the snake venom, and she survived. This summer
she will be vacationing in the same area. Should she get a booster
shot against snakebite before her vacation? No, because it is not a
virus so you cannot get memory cells. No booster for passive immunity.
Booster is a weakened virus that you inject and provokes an immune
response.

A new patient presents at the clinic with the following history: A CD4
cell count of 500, generalized lymphadenopathy, and a positive HIV
test 8 years ago. What phase of HIV infection is the patient in?

A. Primary infection phase

B. Latent phase

C. Conversion phase

D. Overt AIDS phase

A 29-year-old male presents at the clinic complaining of severe

fatigue, night sweats and fever. He reports having multiple sexual
partners and unprotected sex. HIV/AIDS is suspected. What
diagnostic test would be ordered?
 A. PCR

B. EIA

C. Western Blot assay

D. Complete metabolic panel

If a person is on HAART, what should their viral load be? Viral load
(the virus) should be around 0 or not measurable because the medicine is
working against this virus, this means the medicine is working.

If the viral load is increasing, what does that tell you? This means that
the person has become resistant.

A woman's baby is HIV positive.

A. Does this mean the baby has HIV? No, the baby can be HIV positive
and not have HIV. How can you confirm the baby has HIV? PCR-
shows the virus and not the antibodies.

B. Does it mean the father has HIV? the mother? Mother definitely has
HIV.

C. The woman says that since her immunity went to her baby, the baby
will not need any vaccinations. Is this correct? No the baby still needs
vaccinations, passive immunity is temporary.