17: Adaptive Immunity: Specific Defenses of the Host

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17: Adaptive Immunity: Specific Defenses of the Host

Learning Objective

Check Your Understanding

17-1 Differentiate innate from adaptive immunity.

Is vaccination an example of innate or adaptive immunity?

17-2 Differentiate humoral from cellular immunity.

How was basic research on chicken diseases related to the discoveries of both humoral and cellular immunity?

17-3 Define antigen, epitope, and hapten.

Does an antibody necessarily react with a bacterium as an antigen or as an epitope?

17-4 Explain the function of antibodies, and describe their structural and chemical characteristics.

The original theoretical concepts of an antibody called for a rod with antigenic determinants at each end. What is the primary advantage of the Y-shaped structure that eventually emerged?

17-5 Name one function for each of the five classes of antibodies.

Which class of antibody is most likely to protect you from a common cold?

17-6 Compare and contrast T-dependent and T-independent antigens.

Would pneumococcal pneumonia (see Figure 24.13) require a TH cell to stimulate a B cell to form antibodies?

17-7 Differentiate plasma cell from memory cell.

Plasma cells produce antibodies; do they also produce memory cells?

17-8 Describe clonal selection.

In what way does a B cell that encounters an antigen function as an antigen-presenting cell?

17-9 Describe how a human can produce different antibodies.

On what part of the antibody molecule do we find the genetic information that makes the huge genetic diversity of antibody production possible?

17-10 Describe four outcomes of an antigen–antibody reaction.

Antibodies and what other component of the immune system are required for the lysis of a target antigenic cell?

17-11 Describe at least one function of each of the following: M cells, TH1 cells, TH2 cells, TC cells, Treg cells, CTL, NK cells.

What antibody is the primary one produced when an antigen is taken up by an M cell?

17-12 Differentiate T helper, T cytotoxic, and T regulatory cells.

Which T cell is generally involved when a B cell reacts with an antigen and produces antibodies against the antigen?

17-13 Differentiate TH1 and TH2 cells.

Which is the T cell type that is generally involved in allergic reactions?

17-14 Define apoptosis.

What is another name for apoptosis, one that describes its function?

17-15 Define antigen-presenting cell.

Are dendritic cells considered primarily part of the humoral or the cellular immune system?

17-16 Describe the function of natural killer cells.

How does the natural killer cell respond if the target cell does not have MHC class I molecules on its surface?

17-17 Describe the role of antibodies and natural killer cells in antibody-dependent cell-mediated cytotoxicity.

What makes a natural killer cell, which is not immunologically specific, attack a particular target cell?

17-18 Identify at least one function of each of the following cytokines: interleukins, chemokines, interferons, TNF, and hematopoietic cytokines.

What is the function of cytokines?

17-19 Distinguish a primary from a secondary immune response.

Is the anamnestic response primary or secondary?

17-20 Contrast the four types of adaptive immunity.

What type of adaptive immunity is involved when gamma globulin is injected into a person?

Chapter Summary

The Adaptive Immune System (p. 477)

1. An individual’s genetically predetermined resistance to certain diseases is called innate immunity.

2. Adaptive immunity is the ability of the body to specifically react to a microbial infection.

Dual Nature of the Adaptive Immune System (pp. 477–478)

1. Red bone marrow stem cells produce lymphocytes. Lymphocytes that mature in bone marrow become B cells.

2. Humoral immunity involves antibodies, which are found in serum and lymph and are produced by B cells.

3. Lymphocytes that migrate through the thymus become T cells. Cellular immunity involves T cells.

4. T cell receptors recognize antigens.

Antigens and Antibodies (pp. 478–482)

The Nature of Antigens (pp. 478–479)

1. An antigen (or immunogen) is a chemical substance that causes the body to produce specific antibodies.

2. As a rule, antigens are proteins or large polysaccharides. Antibodies are formed against specific regions on antigens called epitopes, or antigenic determinants.

3. A hapten is a low-molecular-weight substance that cannot cause the formation of antibodies unless combined with a carrier molecule; haptens react with their antibodies independently of the carrier molecule.

The Nature of Antibodies (pp. 479–482)

4. An antibody, or immunoglobulin, is a protein produced by B cells in response to an antigen and is capable of combining specifically with that antigen.

5. Typical monomers consist of four polypeptide chains: two heavy chains and two light chains.

6. Within each chain is a variable (V) region that binds the epitope and a constant (C) region that distinguishes the different classes of antibodies.

7. An antibody monomer is Y-shaped or T-shaped: the V regions form the tips, the C regions form the base and FC (stem) region.

8. The FC region can attach to a host cell or to complement.

9. IgG antibodies are the most prevalent in serum; they provide naturally acquired passive immunity, neutralize bacterial toxins, participate in complement fixation, and enhance phagocytosis.

10. IgM antibodies consist of five monomers held by a joining chain; they are involved in agglutination and complement fixation.

11. Serum IgA antibodies are monomers; secretory IgA antibodies are dimers that protect mucosal surfaces from invasion by pathogens.

12. IgD antibodies are on B cells; they may delete B cells that produce antibodies against self.

13. IgE antibodies bind to mast cells and basophils and are involved in allergic reactions.

B Cells and Humoral Immunity (pp. 482–486)

Clonal Selection of Antibody-Producing Cells (pp. 482–488)

1. Red bone marrow stem cells give rise to B cells with IgM and IgD on their surfaces, which recognize specific epitopes.

2. For T-dependent antigens, B cells are selected by antigens with repeating epitopes.

3. For T-independent antigens, B cells are activated by a T cell. The T cell was activated by an antigenic fragment presented with host MHC II.

4. Activated B cells differentiate into plasma cells and memory cells.

5. B cells that recognize self are eliminated by clonal deletion.

The Diversity of Antibodies (p. 484)

6. During development, the genes in embryonic B cells recombine so that mature B cells each have different genes for the V region of their antibodies.

Antigen–Antibody Binding and Its Results (pp. 484–486)

1. An antigen–antibody complex forms when an antibody binds to its specific epitopes on an antigen.

2. Agglutination results when an antibody combines with epitopes on two different cells.

3. Opsonization enhances phagocytosis of the antigen.

4. Antibodies that attach to microbes or toxins cause neutralization.

5. Complement activation results in cell lysis.

T Cells and Cellular Immunity (pp. 486–489)

1. Red bone marrow stem cells give rise to T cells, which mature in the thymus gland. Thymic selection removes T cells that don’t recognize MHC-self molecules.

2. T-cell receptors on T cells recognize antigens.

3. T cells recognize antigens processed by antigen-presenting cells.

4. T cells recognize antigens in association with MHC on an APC.

Classes of T Cells (p. 487)

5. T cells are classified according to their functions and cell-surface glycoproteins called CDs.

T Helper Cells (CD4+ T Cells) (pp. 487–488)

6. TH1 cells activate cells involved in cellular immunity.

7. TH2 cells are associated with allergic reactions and parasitic infections.

8. T helper cells, or CD4+ T cells, are activated by MHC class II on APCs. After binding an APC, CD4+ T cells secrete cytokines that activate other T cells and B cells.

T Cytotoxic Cells (CD8+ T Cells) (pp. 488–489)

9. T cytotoxic cells (TC), or CD8+ T cells, are activated by endogenous antigens and MHC class I on a target cell and are transformed into a CTL.

10. CTLs lyse or induce apoptosis in the target cell.

T Regulatory Cells (p. 489)

11. T regulatory cells (Treg) suppress T cells against self.

Antigen-Presenting Cells (APCs) (pp. 489–490)

1. APCs include B cells, dendritic cells, and macrophages.

2. Dendritic cells are the primary APCs.

3. Activated macrophages are effective phagocytes and APCs.

4. APCs carry antigens to lymphoid tissues where T cells that recognize the antigen are located.

Extracellular Killing by the Immune System (p. 491)

1. Natural killer (NK) cells lyse virus-infected cells, tumor cells, and parasites. They kill cells that do not express MHC class I antigens.

Antibody-Dependent Cell-Mediated Cytotoxicity (pp. 491–492)

1. In ADCC, NK cells and macrophages lyse antibody-coated cells.

Cytokines: Chemical Messengers of Immune Cells (pp. 492–493)

1. Cells of the immune system communicate with each other by means of chemicals called cytokines.

2. Interleukins (IL) are cytokines that serve as communicators between leukocytes.

3. Chemokines cause leukocytes to migrate to an infection.

4. Alpha interferon and IFN- protect cells against viruses. Gamma interferon increases phagocytosis.

5. Tumor necrosis factor promotes the inflammatory reaction.

6. Hematopoietic cytokines promote development of white blood cells.

7. Overproduction of cytokines leads to a cytokine storm, which results in tissue damage.

Immunological Memory (pp. 493–494)

1. The relative amount of antibody in serum is called the antibody titer.

2. The response of the body to the first contact with an antigen is called the primary response. It is characterized by the appearance of IgM followed by IgG.

3. Subsequent contact with the same antigen results in a very high antibody titer and is called the secondary, anamnestic, or memory response. The antibodies are primarily IgG.

Types of Adaptive Immunity (pp. 494–496)

1. Immunity resulting from infection is called naturally acquired active immunity; this type of immunity may be long-lasting.

2. Antibodies transferred from a mother to a fetus (transplacental transfer) or to a newborn in colostrum results in naturally acquired passive immunity in the newborn; this type of immunity can last up to a few months.

3. Immunity resulting from vaccination is called artificially acquired active immunity and can be long-lasting.

4. Artificially acquired passive immunity refers to humoral antibodies acquired by injection; this type of immunity can last for a few weeks.

5. Serum containing antibodies is often called antiserum.

6. When serum is separated by gel electrophoresis, antibodies are found in the gamma fraction of the serum and are termed immune serum globulin, or gamma globulin.

The Loop

Complement is included in Chapter 16 (pp. 463–468).



1. a. Adaptive immunity is the resistance to infection obtained during the life of the individual. Adaptive immunity results from the production of antibodies and T cells. Innate immunity refers to the resistance of species or individuals to certain diseases that is not dependent on antigen-specific immunity.

b. Humoral immunity is due to antibodies (and B cells). Cellular immunity is due to T cells.

c. Active immunity refers to antibodies produced by the individual who carries them. Passive immunity refers to antibodies produced by another source and then transferred to the individual who needs the antibodies.

d. TH1 cells produce cytokines that activate T cells. Cytokines produced by TH2 cells activate B cells.

e. Natural immunity is acquired naturally, i.e., from mother to newborn, or following an infection. Artificial immunity is acquired from medical treatment, i.e., by injection of antibodies or by vaccination.

f. T-dependent antigens: Certain antigens must combine with self-antigens to be recognized by TH cells and then by B cells. T-independent antigens can elicit an antibody response without T cells.

g. T cells can be classified by their surface antigens: TH cells possess the CD4 antigen; TC cells have the CD8 antigen.

h. Immunoglobins = antibodies; TCRs = antigen-receptors on T cells.

2. The major histocompatability complex (MHC) are self-antigens. Th cells react with MHC II; TC cells react with MHC I.


4. See Figure 17.19.

5. T cytotoxic cells (TC) destroy target cells upon contact. T helper cells (TH) interact with an antigen to “present” it to a B cell for antibody formation. Treg cells suppress the immune response. Cytokines are chemicals released by cells that initiate a response by other cells.


7. Both would prevent attachment of the pathogen; (a) interferes with the attachment site on the pathogen and (b) interferes with the pathogen’s receptor site.

8. Rearrangement of the V region genes during embryonic development produces Bcells with different antibody genes.

9. The person recovered because he or she produced antibodies against the pathogen. The memory response will continue to protect the person against that pathogen.

Critical Thinking

1. TC cells secreted TNF and IFN, which diffuse through liver cells and stimulate these cells to produce antiviral proteins.

2. Dietary amino acids are necessary to make antibodies (proteins) and new (T) cells.

3. Having had an M. tuberculosis infection and recovered (naturally acquired active immunity); vaccination with BCG (artificially acquired passive immunity).

4. Antivenin = antibodies against the snake venom; obtained from the serum of a vaccinated horse or mouse (see monoclonal antibodies, pp. 507–509).

Clinical Applications

1. Antibiotics and immunity can cause gram-negative cells to lyse, releasing cell wall fragments. This exposes the body to more endotoxin. The woman’s life-threatening condition was due to endotoxin shock. Monoclonal antibodies removed the cell walls.

2. Increased susceptibility to infection due to decreased antibody formation.

3. He could not produce the secretory component of IgA.

4. The mechanism is called antibody enhancement. Immune complexes of antibodies and viruses attach to cells, facilitating viral penetration.

5. B cells are in the lymph nodes and the spleen.

Copyright © 2010 Pearson Education, Inc.

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