The Body’s Defenses

Immunology Study Guide

Chapter 43

 

 

I.                   Framework

A.  Animal Defense Mechanisms include

1.      nonspecific defenses against variety of microbial attacks

a.       physical – skin and mucous membranes

b.      chemical – lysozyme, gastric juice, interferons, complement

c.       cellular – macrophages, neutrophils, eosinophils, natural killer cells

d.      inflammatory response – histamines, increase blood flow, attract phagocytes; fever

2.      specific defenses against specific foreign invaders

a.       humoral immunity – B cell produce antibodies which bind to antigens to tag foreign cells and molecules which are then destroyed by phagocytes or complement

b.      cell-mediated immunity

                                                                                                   i.      cytotoxic T cells attack infected or cancer cells

                                                                                                 ii.      helper T cells

1.      activate cytotoxic T cells

2.      activate B cells which produce antibodies

II.                Nonspecific Defenses Against Infection

A.     The skin and mucous membranes provide first-line barriers to infection (840-841)

1.      physical barriers to microbes

2.      lysozyme – an enzyme that attaches bacterial cell walls, is present in tears, saliva, and mucus

B.     Phagocytic cells, inflammation, and antimicrobial proteins function early in infection (841-844)

1.      Second line of defense relies on phagocytosis by white blood cells

a.      phagocytic and natural killer cells

1.      neutrophils leave blood and enter infected tissue in response to chemical signals (chemotaxis) and phagocytize microbes

2.      monocytes migrate into tissues and develop into macrophages – large, long-lived amoeboid cells

3.      eosinophils are leukocytes that attack larger parasitic invaders

4.      natural killer cells destroy the body’s infected or abnormal cells by attacking their membranes. 

b.      the inflammatory response – chemical signals released from microbes or from body cells in response to injury initiate inflammatory response

1.      basophils in blood and mast cells in connective tissue release histamine

2.      leukocytes and damaged tissue cells release prostaglandins

3.      vasodilation and chemotactic factors (chemokines) result in congregation of phagocytic cells.

4.      fever stimulates phagocytosis and inhibit growth of microorganisms

c.       antimicrobial proteins

1.      complement system – group of about 20 serum proteins that cooperate with both nonspecific and specific defense mechanisms, resulting in lysis of microbes or attraction of phagocytes

2.      interferons – proteins produced by virus-infected cells that diffuse to neighboring cells, stimulating production of proteins that inhibit viral reproduction in those cells.

 

 

Question:

Complete the table:

 

Cells or Compounds

Functions

Neutrophils

 

Monocytes

 

Macrophages

 

Eosinophils

 

Natural killer cells

 

Basophils and mast cells

 

Histamine

 

Interferons

 

Complement system

 

Lysozyme

 

Prostaglandins

 

Pyrogens

 

Chemokines

 

 

III.             How Specific Immunity Arises

A.     Lymphocytes provide the specificity and diversity of the immune system (844-845)

1.      B lymphocytes (B cells) and T lymphocytes (T cells) – circulate in blood and lymph and are concentrated in the spleen and lymph nodes

a.       both display specificity in their ability to recognize and respond to a particular antigen

b.      certain B cells secrete specific antibodies that interact with specific antigens

c.       B and T cells have membrane-bound antigen receptors:  transmembrane antibodies in B cells and T cells receptors, which are structurally related to membrane antibodies but are never produced to be secreted.

2.      Antigens interact with specific lymphocytes, inducing immune responses and immunological memory (845-846)

a.       When antigens interact with receptors on specific B or T cells, those lymphocytes activate to divide and differentiate into two clones

1.      effector cells – short-lived cells that combat antigen

2.      memory cells – long-lived cells which carry receptor for antigen

3.      clonal selection – a small number of cells are selected by their interaction with a specific antigen to produce thousands of cells keyed to that particular antigen

 

 

b.      immune response

1.      primary immune response – takes 10 – 17 days for selected lymphocytes to proliferate and differentiate to yield the maximum response

2.      secondary immune response – (immunological memory) provides long-term protection to previously encountered pathogen

3.      Lymphocyte development gives rise to an immune system that distinguishes self from nonself (846-847)

a.       immune tolerance for self

b.      role of cell surface markers in T cell function and development

1.      major histocompatability complex (MHC)

a.       Class I MHC – found on all nucleated cells

b.      Class II MHC – found on macrophages, B cells, activated T cels, and cells of the interior thymus

c.       MHC coding alleles result in a unique biochemical fingerprint

2.      Role of MHC molecules – antigen presentation to T cells

a.       antigen receptors of cytotoxic T cells (TC) bind to fragments of antigens displayed by body’s class I MHC molecules

b.      receptors of helper T cells (TH) bind to antigens displayed by body’s class II MHC molecules

c.       differentiation of TC or TH in the thymus depends on their affinity for class I MHC or class II MHC molecules

 

Question:

Describe the four attributes that characterize the immune system.

1.

 

2.

 

3.

 

4.

 

IV.              Immune Responses

A.     Helper T lymphocytes function in both humoral and cell-mediated immunity (849-850)

1.      Antigen-presenting cells (APCs) – B cells and macrophages that present fragments of antigens in their class II MHC molecules to helper T cells.

a.       CD4 – T cell surface protein that enhances interaction between and APC and helper T cell, which results in the proliferation and differentiation of a clone of activated helper T cells and memory helper T cells

b.      Helper T cells secrete cytokines, such as interleukin-2 (IL-2), which helps activate B cells and cytotoxic T cells

c.       Antigen-presenting macrophage secretes interleukin (IL-1), which activates the helper T cell to produce cytokines

d.      Suppressor T cell (TS) may suppress the immune response when the antigen is no longer present

B.     Cytotoxic T cells counter intracellular pathogens in the cell-mediated response (850-851)

1.      Viral infected cells expose viral peptides in its class I MHC molecules.

2.      CD8 surface proteins on CT cells have an affinity for class I MHC molecules and enhance interaction between infected or tumor cells

3.      IL-2 released from TH cells stimulated activation of CT into killer cells which release perforin

 

Questions:

a.  What surface molecule of a helper T cell facilitates the interaction with a class II MHC of an APC and the helper T cell?

 

 

b.  What surface molecule on a cytotoxic T cell assists in the interaction with class I MHC proteins displayed on infected cells?

 

 

c.  What does an activated helper T cell release?

 

 

d.  What does a cytotoxic T cell attached to an infected body cell release?

 

 

C.     B cells make antibodies against extracellular pathogens in the humoral response (851-852)

1.      Activation of B cells is aided by IL-2 and other cytokines released from helper T cells

2.      B cells proliferate into clone of plasma cells and clone of memory B cells

3.      T-dependent antigens – protein antigens that require the aid of helper T cells to stimulate antibody production

4.      T-independent antigens – trigger antibody production by B cells without the aid of IL-2

 

Questions:

a.  How do B cells serve as APCs?

 

 

b.  Why is it thought that B cells function as important APCs in the secondary response to an antigen but not in the primary response to that antigen?

 

 

D.     Antibody structure and function

1.      Antibodies recognize a localized region (epitope) of an antigen.  Antigens may have many different epitopes that stimulate different B cells to produce antibodies.

2.      Antibodies are a class of proteins called immunoglobulins (Igs)

3.      Y-shaped molecules that consists of four polypeptide chains:  two identical light chains and two identical heavy chains.

a.       linked by disulfide bridges

b.      variable region at the end of the Y provide antigen specificity.

4.      five types of heavy chain constant regions in the tail of the Y-shaped antibody:  creates five classes of antibodies:  IgM, IgG, IgA, IgD, and IgE

5.      Monoclonal antibodies – identical antibodies used in biological research, clinical testing and medical applications

E.      Antibody-mediated disposal of antigens

1.      neutralization – antibodies block the activity of an antigen, as when antibodies cover the binding sites of a virus

2.      opsonization – antibodies coat microbes and enhance phagocytosis by macrophages

3.      agglutination – antibody-antigen complex that cause soluble antigen molecules to precipitate.  Resulting clumps are engulfed by phagocytes

4.      complement fixation – antigen-antibody complex may activate complement system.

a.       classical pathway (humoral response) – complement proteins form a membrane attack complex, which lyses pathogen

b.      alternative pathway (nonspecific immune response) – complement proteins amplify inflammatory response

1.      by stimulating release of histamine from basophils and mast cells.

2.      attracting phagocytes to infection site

3.      coat microorganisms, stimulating phagocytosis

 

Question:

List four ways in which antibodies mediate the disposal of antigens.  Which of these enhance phagocytosis by macrophages?

1.

 

2.

 

3.

 

4.

 

V.                 Immunity in Health and Disease

A.     Immunity can be achieved naturally or artificially (855-857)

1.      Active immunity – acquired when body produces antibodies and develops immunological memory from either exposure and recovery from an infection or from immunization

2.      Passive immunity – temporary immunity provided by antibodies supplied through the placenta, breast milk or antibody injection

B.     Limits to blood transfusion and tissue transplantation (857-858)

1.      Blood groups and blood transfusion – ABO blood group antigens trigger antibody production when introduced to a body possessing different antigens.  Anti-blood group antibodies are in the IgM class and do not cross the placenta.

2.      Rh-negative mother may develop antibodies against the Rh factor if fetal blood from an Rh-positive child leaks across the placenta.

a.       immunological memory may result in the production of IgG antibodies that can cross the placenta and destroy fetal red blood cells.

b.      Treatment of mother with anti-Rh antibodies just after delivery destroys any Rh antigen that may have leaked into her circulation.

3.      Tissue Grafts and Organ Transplantation

a.       transplanted tissues and organs are rejected because the foreign MHC molecules are antigenic and trigger immune response

b.      use of closely related donors and drugs (cyclosporine A and FK506) that suppress cell-mediated immunity help reduce the immune response