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CHAPTER
21
The Immune System: Innate
and Adaptive Body Defenses
Objectives
Part 1: Innate Defenses
Surface Barriers: Skin and Mucosae
1. Describe surface membrane barriers and their protective functions.
Internal Innate Defenses: Cells and Chemicals
2. Explain the importance of phagocytosis and natural killer cells in innate body defense.
Part 2: Adaptive Defenses
Antigens
6. Define antigen and describe how antigens affect the adaptive defenses.
7. Define complete antigen, hapten, and antigenic determinant.
Cells of the Adaptive Immune System: An Overview
Humoral Immune Response
11. Define humoral immunity.
15. Describe the structure of an antibody monomer, and name the five classes of antibodies.
16. Explain the function(s) of antibodies and describe clinical uses of monoclonal antibodies.
Cellular Immune Response
17. Define cellular immunity and describe the process of activation and clonal selection of
T cells.
Homeostatic Imbalances of Immunity
22. Give examples of immunodeficiency diseases and of hypersensitivity states.
23. Cite factors involved in autoimmune disease.
Developmental Aspects of the Immune System
Suggested Lecture Outline
Part 1: Innate Defenses (pp. 765–773; Figs. 21.1–21.6; Tables
21.1–21.2)
I. Surface Barriers: Skin and Mucosae (pp. 765–766; Fig. 21.1)
A. Skin, a highly keratinized epithelial membrane, represents a physical barrier to most
microorganisms and their enzymes and toxins (p. 765).
II. Internal Innate Defenses: Cells and Chemicals (pp. 766–773; Figs. 21.2–21.6;
Tables 21.1–21.2)
A. Phagocytes, such as neutrophils and macrophages, confront microorganisms that breach
the external barriers (p. 766; Fig. 21.2).
1. Phagocytes must be able to adhere to a pathogen before it can engulf it; to counteract
this, pathogens are coated with complement proteins called opsonins.
B. Natural killer cells are able to lyse and kill cancer cells and virally infected cells before
the adaptive immune system has been activated (pp. 766–767).
C. Inflammation occurs any time the body tissues are injured by physical trauma, intense
heat, irritating chemicals, or infection by viruses, fungi, or bacteria (pp. 767–771; Figs.
21.3–21.4; Table 21.1).
1. Inflammation is beneficial because it prevents the spread of damage, disposes of
debris and pathogens, alerts the adaptive immune system, and sets up repair.
tissues.
4. Soon after inflammation, the damaged site is invaded by neutrophils and macrophages.
a. Injured cells produce leukocytosis-inducing factors that induce neutrophils to enter
the blood from the bone marrow, increasing their number.
D. Antimicrobial proteins enhance the innate defenses by attacking microorganisms directly
or by hindering their ability to reproduce (pp. 771–773; Figs. 21.5–21.6; Table 21.2).
1. Interferons are small proteins produced by virally infected cells that help protect
surrounding healthy cells (p. 771; Fig. 21.5; Table 21.2).
2. Complement refers to a group of about 20 plasma proteins that provide a major mecha-
nism for destroying foreign pathogens in the body (pp. 771–773; Fig. 21.6; Table 21.2).
E. Fever, or an abnormally high body temperature, is a systemic response to microorgan-
isms (p. 773; Table 21.2).
1. Pyrogens produced by leukocytes and macrophages act on the hypothalamus, causing
a rise in body temperature.
Part 2: Adaptive Defenses (pp. 773–796; Figs. 21.7–21.21; Tables
21.3–21.7)
III. Antigens (pp. 773–774; Fig. 21.7)
A. Aspects of the Adaptive Immune Response (pp. 773–774)
1. The adaptive defenses recognize and destroy the specific antigen that initiated the
response.
4. Humoral immunity is provided by antibodies produced by lymphocytes present in the
body’s “humors” or fluids.
5. Cellular immunity is based on direct attack of microorganisms by lymphocytes and
has living cells, rather than free proteins, as its protective factor.
B. Antigens are substances that can mobilize the immune system and provoke an immune
response (pp. 773–774; Fig. 21.7).
1. Complete antigens are able to stimulate the proliferation of specific lymphocytes and
antibodies and to react with the activated lymphocytes and produced antibodies.
IV. Cells of the Adaptive Immune System: An Overview (pp. 774–778; Figs. 21.8–
21.10; Table 21.3)
A. Lymphocytes originate in the bone marrow and, when released, become immunocompe-
tent and self-tolerant in either the thymus (T cells) or the bone marrow (B cells)
(pp. 774–777; Figs. 21.8–21.9).
1. The B lymphocyte selection process is not well understood: the T lymphocytes
undergo selection for immunocompetence by going through two processes:
3. Immune cells in lymphoid organs are well-placed to encounter antigens, so the first
encounter between a lymphocyte and antigens usually occurs there.
a. Antigen binding with a particular lymphocyte selects that lymphocyte for further
development, a process called clonal selection.
B. Antigen-presenting cells (APCs) are responsible for activating T cells, by engulfing
antigens and presenting fragments of these antigens on their surfaces, where they can be
recognized by T cells (pp. 777–778; Fig. 21.10; Table 21.3).
1. Dendritic cells are APCs located on body surfaces that have contact with the external
environment: they phagocytose antigens and migrate to lymphoid organs to present
antigens to T cells.
V. Humoral Immune Response (pp. 778–784; Figs. 21.11–21.15; Table 21.4)
A. The immunocompetent but naive B lymphocyte is activated when antigens bind to its
surface receptors (pp. 778–779; Fig. 21.11).
1. Clonal selection is the process of the B cell growing and multiplying to form an army
of cells that are capable of recognizing the same antigen.
B. Immunological Memory (pp. 779–780; Fig. 21.12)
1. The primary immune response occurs on first exposure to a particular antigen, with a
lag time of about 3–6 days.
a. After mobilization, the antibody titer in the blood rises, peaking in about 10 days,
and then declines to a low level.
C. Active and Passive Humoral Immunity (p. 780; Fig. 21.13)
1. Active immunity occurs when the body mounts an immune response to an antigen.
2. Passive immunity occurs when a person is given preformed antibodies.
a. Naturally acquired passive immunity occurs when a mother’s antibodies enter fetal
circulation.
D. Antibodies or immunoglobulins are proteins secreted by plasma cells in response to an
antigen that are capable of binding to that antigen (pp. 780–784; Figs. 21.14–21.15;
Table 21.4).
1. The basic antibody structure consists of four looping polypeptide chains linked
together by disulfide bonds.
3. Antibody Targets and Functions
a. Complement fixation and activation occurs when complement binds to antibodies
attached to antigens and leads to lysis of the cell.
4. Monoclonal antibodies are commercially prepared antibodies specific for a single
antigenic determinant.
VI. Cellular Immune Response (pp. 784–792; Figs. 21.16–21.20; Tables 21.3,
21.5–21.7)
A. There are two major populations of T cells, based on which of the cell differentiation
glycoproteins the mature cell displays: CD4 cells, and CD8 cells (pp. 784–786;
Fig. 21.16; Table 21.3).
B. MHC proteins presented to T lymphocytes activate them (p. 786; Table 21.5).
1. Class I MHCs are found on all body cells except RBCs and display antigens
synthesized from within the cell; if infected, the MHCs may also include fragments of
foreign antigens.
2. Class II MHCs are only found on cells that present antigens to CD4 cells.
C. Activation and Differentiation of T Cells (pp. 786–787; Fig. 21.17; Table 21.6).
1. When T cell antigen receptors bind an antigen, the cell must accomplish a double
D. Roles of Specific Effector T Cells (pp. 787–790; Figs. 21.18–21.20; Table 21.7)
1. Helper T cells stimulate proliferation of other T cells and B cells that have already
become bound to antigen.
E. Organ Transplants and Prevention of Rejection (pp. 790–792)
1. Grafts
a. Autografts are tissue grafts transplanted from one body site to another in the same
person.
2. Transplant success depends on the similarity of the tissues because cytotoxic T cells,
NK cells, and antibodies work to destroy foreign tissues.
VII. Homeostatic Imbalances of Immunity (pp. 792–796; Fig. 21.21)
A. Immunodeficiencies are any congenital or acquired conditions that cause immune cells,
phagocytes, or complement to behave abnormally (pp. 792–794).
1. Severe combined immunodeficiency (SCID) is a congenital condition that produces a
deficit of B and T cells.
C. Hypersensitivities result when the immune system causes tissue damage as it fights off a
perceived threat that would otherwise be harmless (pp. 794–796; Fig. 21.21).
1. Immediate hypersensitivities (acute, or type I hypersensitivities), or allergies, begin
within seconds after contact and last about half an hour.
2. Subacute hypersensitivities are caused by antibodies, take 1–3 hours to occur, and last
10–15 hours.
a. Cytotoxic (type II) reactions occur when antigens bind to antigens on specific body
3. Delayed hypersensitivity reactions are caused by T lymphocytes, can take 1–3 days to
occur, and may take weeks to go away.
VIII. Developmental Aspects of the Immune System (p. 796)
A. Stem cells of the immune system originate in the liver and spleen during weeks 1–9 of
embryonic development; later the bone marrow takes over this role.
Cross References
Additional information on topics covered in Chapter 21 can be found in the chapters listed below.
1. Chapter 2: Protein structure
2. Chapter 3: Cilia; lysosomes
3. Chapter 5: Mechanical and chemical protection of the skin; dendritic cells
of mucous barriers; stellate macrophages
9. Chapter 24: Body temperature regulation
10. Chapter 28: Antibody protection of the fetus due to maternal antibodies
Lecture Hints
1. Although specific and nonspecific defense mechanisms are treated as separate entities,
2. Point out that the body has several lines of defense—mechanical, chemical, and cellular.
3. Students often have difficulty in determining which mechanisms are specific and which
4. Emphasize the logic behind the four cardinal signs of inflammation. For example, to
bring the large quantities of oxygen and nutrients for repair processes, blood supply to an
6. To illustrate the action of pyrogens on the hypothalamus, use the example of resetting the
7. Mention that cytotoxic T cells must come in contact with the invader, but that B cells
send out antibodies from sometimes remote locations to target specific antigens.
9. To reinforce the idea of clonal selection, point out that a single B cell could not possibly
produce enough antibody to neutralize a large quantity of antigen, but having many B
10. Stress that with active vs. passive immunity, the source of the antibodies is irrelevant;
11. In the discussion of complement, ask the class, “What would happen if an antibody
bound to a completely normal body cell?” Use this as a lead-in to the topic of comple-
ment recognition of the constant region of the antibody.
Activities/Demonstrations
1. Audiovisual materials are listed in the Multimedia in the Classroom and Lab section of
this Instructor Guide (p. 387).
Critical Thinking/Discussion Topics
1. Discuss the pros and cons of using immunizations for mumps, measles, etc.
2. Explore the autoimmune diseases, how they occur, symptoms, prognosis, and treatment.
3. Discuss why some individuals are sensitive (allergic) to drugs from one source, but are
not so sensitive to drugs from another source.
7. Explain why we need specific resistance mechanisms even though nonspecific resistance
mechanisms attack all foreign substances (i.e., why is specific resistance necessary at
all?).
8. Explain what the body’s immune response is to an antitoxin or other passive
immunization.
9. Discuss why chemotherapeutics attached to monoclonal antibodies are an advantage over
injection of the chemical agent alone. Could there be any drawbacks to this therapy?
Library Research Topics
1. Research some of the opportunistic diseases that often accompany AIDS.
2. Study the difficulties involved in transplant surgeries.
List of Figures and Tables
All of the figures in the main text are available in JPEG format, PPT, and labeled & unlabeled
format on the Instructor Resource DVD. All of the figures and tables will also be available in
Transparency Acetate format. For more information, go to www.pearsonhighered.com/educator.
Figure 21.1 Overview of innate and adaptive defenses.
Figure 21.2 Phagocytosis.
Figure 21.3 Inflammation: flowchart of events.
Figure 21.8 Lymphocyte development, maturation, and activation.
Figure 21.9 T cell education in the thymus.
Figure 21.10 Dendritic cell.
Figure 21.11 Clonal selection of a B cell.
Figure 21.12 Primary and secondary humoral responses.
Figure 21.13 Active and passive humoral immunity.
Figure 21.18 The central role of helper T cells in mobilizing both humoral
and cellular immunity.
Figure 21.19 Cytotoxic T cells attack infected and cancerous cells.
Figure 21.20 Simplified summary of the primary immune response.
Figure 21.21 Mechanism of an acute allergic (immediate hypersensitivity)
response.
Answers to End-of-Chapter Questions
Multiple-Choice and Matching Question answers appear in Appendix H of the main text.
Short Answer Essay Questions
13. Mucosae are found on the outer surface of the eye and in the linings of all body cavities
open to the exterior, such as the digestive, respiratory, urinary, and reproductive tracts.
The epidermis is the outermost covering of the body surface. Mucus provides a sticky
mechanical barrier that traps pathogens.
14. Attempts at phagocytosis are not always successful because to accomplish ingestion, the
phagocyte must first adhere to the particle. Complement proteins and antibodies coat
foreign particles, providing binding sites to which phagocytes can attach, making phago-
cytosis more efficient. (p. 766)
15. The term complement refers to a heterogenous group of at least 20 plasma proteins that
normally circulate in an inactive state. Complement is activated by one of three pathways:
classical, lectin, or alternative, all involving the plasma proteins. Each pathway involves a
Other roles of complement include opsonization, inflammatory actions such as stimulat-
ing mast cells and basophils to release histamine (which increases vascular permeability),
and attracting neutrophils and other inflammatory cells to the area. (pp. 771–773)
16. Interferons are secreted by virus-infected cells. They diffuse to nearby cells where
17. Humoral immunity is provided by the antibodies in the body’s fluids. Cellular
immunity is provided by non–antibody-producing lymphocytes, i.e., T cells. (p. 773)
18. Cytokines released by helper T cells help to amplify and regulate both the humoral and
19. Immunocompetence is the ability of the immune system’s cells to recognize foreign
20. A primary immune response results in cellular proliferation, differentiation of mature
effector and memory lymphocytes, and the synthesis and release of antibodies—a series
21. Antibodies are proteins secreted by plasma cells in response to a specific antigen, and
they are capable of binding to that antigen. See Figure 21.14 for a look at basic antibody
structure. (p. 781)
22. The variable region of an antibody is the portion of the antibody that binds to the
different antigens. There is a different variable region for each different antigen. The
23. The antibody classes and their probable locations in the body include the following:
Class IgD—virtually always attached to B cells; B cell receptor
Class IgM—monomer attached to B cells; pentamer free in plasma (during primary
24. Antibodies help defend the body by complement fixation, which activates complement
proteins, neutralization, which binds antigens and removes them from the circulating
25. Vaccines produce active humoral immunity because most contain dead or extremely
weakened pathogens that have the antigenic determinants necessary to stimulate the
immune response but are generally unable to cause disease. Passive immunity is less than
satisfactory because neither active antibody production nor immunological memory is
established. (p. 780)
26. Activation of CD4 cells involves both antigen binding and co-stimulation. The CD4 cells
bind only to antigen linked to class II MHC proteins, typically found on the surface of
27. Helper T cells function to chemically or directly stimulate the proliferation of other
T cells and of B cells that have already become bound to antigen. Regulatory T cells
28. Cytokines are soluble glycoproteins released by activated T cells. They enhance the
defensive activity of T cells, B cells, and macrophages. Specific cytokines and their role
in the immune response are summarized in Table 21.6. (p. 790)
29. Hypersensitivity is an antigen-induced state that results in abnormally intense immune
responses to an innocuous antigen. Immediate hypersensitivities include anaphylactic
30. Autoimmune disease results from changes in the structure of self-antigens, ineffective or
inefficient lymphocyte programming, and by cross-reaction of antibodies produced
against foreign antigens with self-antigens. (p. 794)
Critical Thinking and Clinical Application Questions
1. a. Jenny has severe combined immunodeficiency disease (SCID), in which T cells and
B cells fail to develop. At best there are only a few detectable lymphocytes. If left
untreated, this condition is fatal.
b. Jenny’s brother has the closest antigenic match, as both children are from the same
2. IgA is found primarily in mucus and other secretions that bathe body surfaces. It plays an
3. The leaking of plasma proteins into the interstitial fluid causes an increase in the osmotic
pressure, resulting in additional fluid leaking from the plasma and localized edema. This
4. Costanza was exhibiting the typical signs of an immediate hypersensitivity response.
5. The HIV virus is transferred from the mother to the baby through the placenta. Caroline’s
helper T cells are infected. This is devastating to the immune response because of the
role of the helper T cells in activating both the humoral immune response of the B cells
Suggested Readings
Amin, Kawa. “The Role of Mast Cells in Allergic Inflammation.” Respiratory Medicine 106
(1) (Jan. 2012): 9–14.
Brown, Phyllida. “Cinderella Goes to the Ball.” Nature 410 (6832) (April 2001): 1018–1020.
Carroll, Maria V., and Robert B. Sim. “Complement in Health and Disease.” Advanced Drug
Delivery Reviews 63 (12) (Sept. 2011): 965–975.
2011): 317–329.
Gura, Trisha. “Innate Immunity: Ancient System Gets New Respect.” Science 291 (5511)
(March 2002): 2068–2071.
King, Leslie B., and John G. Monroe. “B Cell Receptor Rehabilitation—Pausing to Reflect.”
Science 291 (5508) (Feb. 2001): 1503–1506.
Kloetzel, Peter M. “Antigen Processing by the Proteasome.” Nature Reviews: Molecular Cell
Biology 2 (3) (March 2001): 179–193.
Marano, Daniel A. “Soil Salvation.” Psychology Today 41 (5) (Sept./Oct. 2008): 57–58.
Marshall, Eliot. “Lupus: Mysterious Disease Holds its Secrets Tight.” Science 296 (5568)
(April 2002): 689–691.
McCune, Joseph N. “The Dynamics of CD4+ T-Cell Depletion.” Nature 410 (6831)
(April 2001): 1002–1007.
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974–979.
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Rossig, Claudia. “Anti-Tumor Cytotoxic T Lymphocytes Targeting Solid Tumors: Ready for
Clinical Trials.” Cytotherapy 14 (1) (Jan. 2012): 4–6.
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2001): 2370–2376.
