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The Immune System

by
Edition:
2nd
ISBN13:

9780815340935

ISBN10:
0815340931
Format:
Paperback
Pub. Date:
5/25/2004
Publisher(s):
ROUTLEDGE
List Price: $116.00
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Summary

The Immune System, Second Edition has been designed for use in immunology courses for undergraduate, medical, dental, and pharmacy students. This class-tested and successful textbook synthesizes the established facts of immunology into a comprehensible, coherent, and up-to-date account of how the immune system works, rather than presenting immunology as a chronology of experiments and discoveries. Emphasizing the human immune system the text has been designed to break down the barriers which often divide basic and clinical immunology. The reader-friendly text, section and chapter summaries, and full-color illustrations make the book accessible and easily understandable to students.The Immune Systemis adapted fromImmunobiologyby Janeway, Travers & Walport. New in the Second Edition: -Inclusion of end-of-chapter questions throughout the book. Questions consist of a mix of clinical and basic science. Detailed answers to all questions are provided in the back of thebook. -Completely updated throughout. -Even greater emphasis on human immunity. -Enhanced and revised treatment of the complement system, including new figures and icons to clarify concepts. -Increased emphasis on human genetics throughout the book. -Expanded and updated treatment of innate immunity, particularly the mucosal system.

Author Biography

Peter Parham is on the faculty at Stanford University where he is a Professor in the Departments of Structural Biology, and Microbiology and Immunology.

Table of Contents

Elements of the Immune System and their Roles in Defense
1(36)
Defenses facing invading pathogens
2(1)
Pathogens are infectious organisms that cause disease
2(3)
The skin and mucosal surfaces form physical barriers against infection
5(2)
The innate immune response causes inflammation at sites of infection
7(1)
The adaptive immune response adds to an ongoing innate immune response
8(3)
Immune system cells with different functions all derive from hematopoietic stem cells
11(4)
Most lymphocytes are present in specialized lymphoid tissues
15(1)
Lymphocytes are activated in the secondary lymphoid tissues
16(5)
Summary
20(1)
Principles of adaptive immunity
20(1)
Immunoglobulins and T-cell receptors are the highly variable recognition molecules of adaptive immunity
21(1)
The diversity of immunoglobulins and T-cell receptors is generated by gene rearrangement
22(1)
B cells recognize intact pathogens, whereas T cells recognize pathogen-derived peptides bound to proteins of the major histocompatibility complex
23(1)
Clonal selection of B and T lymphocytes is the guiding principle of the adaptive immune response
24(2)
Extracellular pathogens and their toxins are eliminated by antibodies
26(2)
Adaptive immune responses generally give rise to long-lived immunological memory and protective immunity
28(1)
The immune system can be compromised by inherited immunodeficiencies or by the actions of certain pathogens
29(1)
Unwanted effects of adaptive immunity cause allergy, autoimmune disease, and rejection of transplanted tissues
30(7)
Summary
32(1)
Summary to Chapter 1
33(1)
Questions
34(3)
Antibody Structure and the Generation of B-Cell Diversity
37(30)
The structural basis of antibody diversity
38(1)
Antibodies are composed of polypeptides with variable and constant regions
38(2)
Immunoglobulin chains are folded into compact and stable protein domains
40(1)
An antigen-binding site is formed from the hypervariable regions of a heavy-chain and a light-chain V domain
41(1)
Antigen-binding sites vary in shape and physical properties
42(3)
Monoclonal antibodies are produced from a clone of antibody-producing cells
45(3)
Summary
47(1)
Generation of immunoglobulin diversity in B cells before encounter with antigen
47(1)
The DNA sequence encoding a V region is assembled from two or three gene segments
48(1)
Random recombination of gene segments produces diversity in the antigen-binding sites of immunoglobulins
49(2)
Recombination enzymes produce additional diversity in the antigen-binding sites of immunoglobulins
51(1)
Naive B cells use alternative mRNA splicing to make both IgM and IgD
52(1)
Each B cell produces immunoglobulin of a single antigen specificity
52(2)
Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface
54(1)
Summary
54(1)
Diversification of antibodies after B cells encounter antigen
55(1)
Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing
55(1)
Rearranged V-region sequences are further diversified by somatic hypermutation
56(1)
Isotype switching produces immunoglobulins with different C regions but identical antigen specificities
57(1)
Antibodies with different C regions have different effector functions
58(9)
Summary
61(1)
Summary to Chapter 2
61(2)
Questions
63(4)
Antigen Recognition by T Lymphocytes
67(32)
T-cell receptor diversity
68(1)
The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin
68(1)
T-cell receptor diversity is generated by gene rearrangement
69(2)
Expression of the T-cell receptor on the cell surface requires association with additional proteins
71(1)
γ and δ chains form a second class of T-cell receptor expressed by a distinct population of T cells
71(3)
Summary
73(1)
Antigen processing and presentation
73(1)
Two classes of T cell are specialized to respond to intracellular and extracellular sources of infection
74(1)
Two classes of MHC molecule present antigen to CD8 and CD4 T cells respectively
75(1)
The two classes of MHC molecule have similar three-dimensional structures
76(1)
MHC molecules bind a variety of peptides
77(1)
Peptides generated in the cytosol are transported into the endoplasmic reticulum where they bind MHC class I molecules
78(2)
Peptides presented by MHC class II molecules are generated in acidified intracellular vesicles
80(2)
MHC class II molecules are prevented from binding peptides in the endoplasmic reticulum by the invariant chain
82(1)
The T-cell receptor specifically recognizes both peptide and MHC molecule
83(1)
The two classes of MHC molecule are expressed differentially on cells
83(3)
Summary
85(1)
The major histocompatibility complex
86(1)
The diversity of MHC molecules in the human population is due to multigene families and genetic polymorphism
86(1)
The MHC class I and class II genes occupy different regions of the MHC
87(1)
Other proteins involved in antigen processing and presentation are encoded in the MHC class II region
88(1)
MHC polymorphism affects the binding and presentation of peptide antigens to T cells
89(1)
MHC diversity results from selection by infectious disease
90(3)
MHC polymorphism triggers T-cell reactions that can reject transplanted organs
93(6)
Summary
94(1)
Summary to Chapter 3
95(1)
Questions
95(4)
The Development of B Lymphocytes
99(12)
The development of B cells in the bone marrow
99(1)
B-cell development in the bone marrow proceeds through several stages
100(2)
The survival of a developing B cell depends on the productive rearrangement of a heavy- and a light-chain gene
102(3)
Cell-surface expression of the products of rearranged immunoglobulin genes prevents further gene rearrangement
105(1)
The proteins involved in immunoglobulingene rearrangement are controlled developmentally
106(2)
Many B-cell tumors carry chromosomal translocations that join immunoglobulin genes to genes regulating cell growth
108(1)
B cells expressing the glycoprotein CD5 express a distinctive repertoire of receptors
108(3)
Summary
110(1)
Selection and further development of the B-cell repertoire
110(1)
Self-reactive immature B cells are altered, eliminated, or inactivated by contact with self-antigens
111(12)
Mature, naive B cells compete for access to lymphoid follicles
112(1)
Encounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells
113(2)
Different types of B-cell tumor reflect B cells at different stages of development
115(8)
Summary
116(1)
Summary to Chapter 4
117(2)
Questions
119(4)
The Development of T Lymphocytes
123(22)
The development of T cells in the thymus
124(1)
T cells develop in the thymus
124(1)
The two lineages of T cells arise from a common thymocyte progenitor
125(1)
Production of a T-cell receptor β chain leads to cessation of β-chain gene rearrangement and to expression of CD4 and CD8
126(3)
T-cell receptor α-chain genes can undergo several successive rearrangements
129(2)
Cells expressing particular γ:δ receptors arise first in embryonic development
131(1)
Summary
131(1)
Positive and negative selection of the T-cell repertoire
131(1)
T cells that can recognize self-MHC molecules are positively selected in the thymus
132(1)
Positive selection controls expression of the CD4 or CD8 co-receptor
133(1)
Rearrangement of α-chain genes stops once a cell has been positively selected
134(1)
T cells specific for self-antigens are removed in the thymus by negative selection
135(1)
T cells undergo further differentiation in secondary lymphoid tissues after encounter with antigen
136(1)
The requirements of thymic selection can limit the number of functional class I and class II genes in the MHC
137(2)
Most T-cell tumors represent early or late stages of T-cell development
139(6)
Summary
139(1)
Summary to Chapter 5
140(2)
Questions
142(3)
T Cell-Mediated Immunity
145(36)
Activation of naive T cells on encounter with antigen
145(1)
Dendritic cells carry antigens from sites of infection to secondary lymphoid tissues
146(1)
Naive T cells first encounter antigen on antigen-presenting cells in secondary lymphoid tissues
147(1)
Homing of naive T cells to secondary lymphoid tissues is determined by cell adhesion molecules
148(2)
Activation of naive T cells requires a co-stimulatory signal delivered by a professional antigen-presenting cell
150(1)
Secondary lymphoid tissues contain three kinds of professional antigen-presenting cell
151(4)
When T cells are activated by antigen, signals from T-cell receptors and co-receptors alter the pattern of gene transcription
155(3)
Proliferation and differentiation of activated T cells are driven by the cytokine interleukin-2
158(1)
Antigen recognition by a naive T cell in the absence of co-stimulation leads to the T cell becoming nonresponsive
159(1)
On activation, CD4 T cells can acquire different helper functions
159(1)
Naive CD8 T cells can be activated in different ways to become cytotoxic effector cells
160(1)
Summary
161(2)
The properties and functions of effector T cells
163(1)
Effector T cells can be stimulated by antigen in the absence of co-stimulatory signals
163(1)
Effector T-cell functions are performed by cytokines and cytotoxins
164(1)
Cytotoxic CD8 T cells are selective and serial killers of target cells at sites of infection
165(3)
Cytotoxic T cells kill their target cells by inducing apoptosis
168(1)
TH1 CD4 cells induce macrophages to become activated
169(2)
TH1 cells coordinate the host response to intravesicular pathogens
171(1)
CD4 TH2 cells activate only those B cells that recognize the same antigen as they do
172(1)
Regulatory CD4 T cells limit the activities of effector CD4 and CD8 T cells
173(8)
Summary
174(1)
Summary to Chapter 6
175(2)
Questions
177(4)
Immunity Mediated by B Cells and Antibodies
181(46)
Antibody production by B lymphocytes
182(1)
B-cell activation requires cross-linking of surface immunoglobulin
182(1)
The antibody response to certain antigens does not require T-cell help
183(2)
B cells needing T-cell help are activated in secondary lymphoid tissues where they form germinal centers
185(3)
Activated B cells undergo somatic hypermutation and affinity maturation in the specialized microenvironment of the germinal center
188(4)
Interactions with T cells are required for isotype switching in B cells
192(2)
Summary
193(1)
Antibody effector functions
194(1)
IgM, IgG, and IgA antibodies protect the blood and extracellular fluids
194(1)
IgA and IgG are transported across epithelial barriers by specific receptor proteins
195(2)
Antibody production is deficient in very young infants
197(1)
High-affinity IgG and IgA antibodies are used to neutralize microbial toxins and animal venoms
197(2)
High-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells
199(1)
The Fc receptors of hematopoietic cells are signaling receptors that bind the Fc regions of antibodies
200(1)
Phagocyte Fc receptors facilitate the recognition, uptake, and destruction of antibody-coated pathogens
201(1)
IgE binds to high-affinity Fc receptors on mast cells, basophils, and activated eosinophils
202(2)
Fc receptors activate natural killer cells to destroy antibody-coated human cells
204(2)
Summary
205(1)
The antigen--antibody mediated pathway of complement activation
205(1)
Complement components are plasma proteins with various functions
206(1)
C1 uses different polypeptides to bind antibody and to activate complement components
207(2)
Fragments of C2 and C4 associate on the pathogen surface to form the classical C3 convertase
209(1)
Cleavage of C3 yields C3b covalently bound to pathogen surfaces
210(1)
Partial lack of C4 is the most common immune protein deficiency in humans
210(1)
C3b produced by the classical C3 convertase permits the formation of a more powerful alternative C3 convertase
211(1)
Fragments of C3 and C4 on pathogen surfaces are recognized by receptors on various cell types
212(2)
Complement receptors remove immune complexes from the circulation
214(1)
The terminal complement proteins lyse pathogens by forming a membrane pore
215(1)
Small peptides released during complement activation induce local inflammation
216(1)
Regulatory proteins in plasma limit the extent of complement activation
217(3)
Regulatory proteins on human cell surfaces protect them from the effects of complement activation
220(7)
Summary
221(1)
Summary to Chapter 7
222(2)
Questions
224(3)
The Body's Defenses Against Infection
227(52)
Innate immunity
227(1)
Infectious diseases are caused by pathogens of diverse types that live and replicate in the human body
228(4)
Surface epithelia present a formidable barrier to infection
232(1)
Complement activation by the alternative pathway tags microorganisms for destruction
233(3)
Several classes of plasma protein limit the spread of infection
236(1)
Phagocytosis by macrophages provides a first line of cellular defense against invading microorganisms
237(1)
Receptors that detect microbial products signal macrophage activation
238(1)
Activation of resident macrophages induces inflammation at sites of infection
239(4)
Neutrophils are dedicated phagocytes that are summoned to sites of infection
243(1)
The homing of neutrophils to infected tissues is induced by inflammatory mediators
244(2)
Neutrophils are potent killers of pathogens and are themselves programmed to die
246(1)
Inflammatory cytokines raise body temperature and activate hepatocytes to make the acute-phase response
247(3)
Type I interferons inhibit viral replication and activate host defenses
250(2)
NK cells provide an early defense against intracellular infections
252(1)
NK-cell receptors differ in the ligands they bind and the signals they generate
253(2)
Three genetic complexes contribute to NK-cell recognition of `missing-self'
255(3)
Minority subpopulations of B and T cells contribute to innate immunity
258(2)
Summary
259(1)
Adaptive immune responses to infection
260(1)
Adaptive immune responses start with T-cell activation in secondary lymphoid tissues
260(2)
Microfold cells in the gut deliver antigens to Peyer's patches
262(1)
Primary CD4 T-cell responses are influenced by the cytokines made by cells of innate immunity
263(1)
Effector T cells are guided to sites of infection by newly expressed cell adhesion molecules
264(1)
Antibody responses develop in lymphoid tissues under the direction of TH2 cells
265(2)
Antibody secretion by plasma cells occurs at sites distinct from those at which B cells are activated by TH2 cells
267(2)
Summary
268(1)
Immunological memory and the secondary immune response
268(1)
Immunological memory after infection is long lived
269(1)
Pathogen-specific memory B cells are more abundant and make better antibodies than naive B cells
269(1)
T-cell memory is maintained by T cells that have different cell-surface markers from naive T cells
270(2)
Maintenance of immunological memory does not require stimulation with antigen
272(1)
The second and subsequent responses to a pathogen are mediated solely by memory lymphocytes and not by naive lymphocytes
273(6)
Summary
275(1)
Summary to Chapter 8
275(1)
Questions
276(3)
Failures of the Body's Defenses
279(32)
Evasion and subversion of the immune system by pathogens
279(1)
Genetic variation within some species of pathogen prevents effective long-term immunity
280(1)
Mutation and recombination allow influenza virus to escape from immunity
280(1)
Trypanosomes use gene rearrangement to change their surface antigens
281(2)
Herpes viruses persist in human hosts by hiding from the immune response
283(1)
Certain pathogens sabotage or subvert immune defense mechanisms
284(2)
Bacterial superantigens stimulate a massive but ineffective T-cell response
286(1)
Immune responses can contribute to disease
286(1)
Summary
287(1)
Inherited immunodeficiency diseases
287(1)
Most inherited immunodeficiency diseases are caused by recessive gene defects
287(2)
Antibody deficiency leads to an inability to clear extracellular bacteria
289(2)
Diminished antibody production also results from inherited defects in T-cell help
291(1)
Defects in complement components impair antibody responses and cause the accumulation of immune complexes
291(1)
Defects in phagocytes result in enhanced susceptibility to bacterial infection
292(2)
Defects in T-cell function result in severe combined immune deficiencies
294(1)
Some inherited immunodeficiencies lead to specific disease susceptibilities
295(1)
Hematopoietic stem cell transplantation is used to correct genetic defects of the immune system
295(2)
Summary
296(1)
Acquired immune deficiency syndrome
296(1)
HIV is a retrovirus that causes slowly progressing disease
297(1)
HIV infects CD4 T cells, macrophages, and dendritic cells
298(1)
Most people who become infected with HIV progress in time to develop AIDS
299(3)
Genetic deficiency of the CCR5 co-receptor for HIV confers resistance to infection
302(1)
HIV escapes the immune response and develops resistance to antiviral drugs by rapid mutation
302(2)
Clinical latency is a period of active infection and renewal of CD4 T cells
304(1)
HIV infection leads to immunodeficiency and death from opportunistic infections
305(6)
Summary
306(1)
Summary to Chapter 9
306(1)
Questions
307(4)
Over-reactions of the Immune System
311(32)
Four types of hypersensitivity reaction are caused by different effector mechanisms of adaptive immunity
311(2)
Type I hypersensitivity reactions
313(1)
IgE binds irreversibly to Fc receptors on mast cells, basophils, and activated eosinophils
313(1)
Tissue mast cells orchestrate IgE-mediated allergic reactions through the release of inflammatory mediators
314(3)
Eosinophils and basophils are specialized granulocytes that release toxic mediators in IgE-mediated responses
317(2)
Mast cells, basophils, and eosinophils can amplify an IgE response started by TH2 cells
319(1)
Common allergens are small proteins inhaled in particulate form that stimulate an IgE response
320(1)
Predisposition to allergy has a genetic basis
321(1)
IgE-mediated allergic reactions consist of an immediate response followed by a late-phase response
322(1)
The effects of IgE-mediated allergic reactions vary with the site of mast-cell activation
323(1)
Systemic anaphylaxis is caused by allergens in the blood
324(1)
Rhinitis and asthma are caused by inhaled allergens
325(1)
Urticaria, angioedema, and eczema are allergic reactions in the skin
326(2)
Food allergies cause systemic effects as well as gut reactions
328(1)
People with parasite infections and high levels of IgE rarely develop allergic disease
328(1)
Allergic reactions are prevented and treated by three complementary approaches
329(2)
Summary
330(1)
Type II, III, and IV hypersensitivity reactions
331(1)
Type II hypersensitivity reactions are caused by antibodies specific for altered components of human cells
331(2)
Type III hypersensitivity reactions are caused by immune complexes formed from IgG and soluble antigens
333(1)
Systemic disease caused by immune complexes can follow the administration of large quantities of soluble antigens
334(2)
Type IV hypersensitivity reactions are mediated by antigen-specific effector T cells
336(7)
Summary
338(1)
Summary to Chapter 10
339(1)
Questions
339(4)
Disruption of Healthy Tissue by the Immune Response
343(36)
Autoimmune diseases
343(1)
The effector mechanisms of autoimmunity resemble those causing certain hypersensitivity reactions
344(2)
Endocrine glands contain specialized cells that are targets for organ-specific autoimmunity
346(1)
Autoimmune diseases of the thyroid can cause either underproduction or overproduction of thyroid hormones
347(1)
The cause of autoimmune disease can be revealed by the transfer of disease with immune effectors
348(2)
Insulin-dependent diabetes mellitus is caused by the selective destruction of insulin-producing cells in the pancreas
350(1)
Autoantibodies against common components of human cells can cause systemic autoimmune disease
351(1)
Most rheumatological diseases are caused by autoimmunity
352(1)
Multiple sclerosis and myasthenia gravis are autoimmune diseases of the nervous system
352(3)
Summary
354(1)
Genetic and environmental factors that predispose to autoimmune disease
355(1)
All autoimmune diseases involve breaking T-cell tolerance
355(1)
Incomplete deletion of self-reactive T cells in the thymus causes autoimmune disease
356(1)
Insufficient control of T-cell co-stimulation favors autoimmunity
357(1)
Regulatory T cells protect cells and tissues from autoimmunity
358(1)
HLA is the dominant genetic factor affecting susceptibility to autoimmune disease
359(2)
Different combinations of HLA class II allotypes confer susceptibility and resistance to diabetes
361(1)
Autoimmunity can be initiated by disease-associated HLA allotypes presenting antigens to autoimmune T cells
362(1)
Noninfectious environmental factors influence the course of autoimmune diseases
363(1)
Loss of oral tolerance leads to inflammation and autoimmunity
364(2)
Infections are environmental factors that can trigger autoimmune disease
366(2)
Autoimmune T cells can be activated in a pathogen-specific or nonspecific manner by infection
368(2)
In the course of autoimmune disease the specificity of the autoimmune response broadens
370(3)
Senescence of the T-cell population can contribute to autoimmunity
373(1)
Do the current increases in hypersensitivity and autoimmune disease have a common cause?
373(6)
Summary
374(1)
Summary to Chapter 11
374(1)
Questions
375(4)
Manipulation of the Immune Response
379(51)
Prevention of infectious disease by vaccination
379(1)
Viral vaccines are made from whole viruses or viral components
380(1)
Bacterial vaccines are made from whole bacteria, their secreted toxins, or capsular polysaccharides
381(2)
Adjuvants nonspecifically enhance the immune response
383(1)
Vaccination can inadvertently cause disease
384(1)
The need for a vaccine and the demands placed on it change with the prevalence of the disease
385(2)
Vaccines have yet to be found for many chronic pathogens
387(2)
Genome sequences of human pathogens open up new avenues of vaccine design
389(1)
A useful vaccine against HIV has yet to be found
390(1)
Summary
390(1)
Transplantation of tissues and organs
391(1)
Transplant rejection and graft-versus-host reaction are immune responses caused by genetic differences between transplant donor and recipient
391(1)
In blood transfusion, donors and recipients are matched for the A,B,O system of blood group antigens
392(2)
Antibodies against A,B,O or HLA antigens cause hyperacute rejection of transplanted organs
394(1)
Anti-HLA antibodies can arise from pregnancy, blood transfusion, or previous transplants
394(1)
Organ transplantation involves procedures that inflame the donated organ and the transplant recipient
395(1)
Acute rejection is caused by effector T cells responding to HLA differences between donor and recipient
396(1)
Chronic rejection of organ transplants is due to the indirect pathway of allorecognition
397(3)
Matching donor and recipient for HLA class I and class II allotypes improves the outcome of transplantation
400(1)
Allogeneic transplantation is made possible by the use of immunosuppressive drugs
400(1)
Corticosteroids change patterns of gene expression
401(2)
Cytotoxic drugs kill proliferating cells
403(1)
Cyclosporin A, tacrolimus, and rapamycin selectively inhibit T-cell activation
404(2)
Antibodies specific for T cells are used to control acute rejection
406(1)
Patients needing a transplant outnumber the available organs
407(1)
Bone marrow transplantation is a treatment for genetic diseases of blood cells
408(1)
The alloreactions in bone marrow transplantation attack the patient, not the transplant
409(2)
The impact of alloreactions on transplantation depends on the type of tissue or organ transplanted
411(1)
Summary
411(1)
Cancer and its interactions with the immune system
412(1)
Cancer results from mutations that cause uncontrolled cell growth
412(2)
A cancer arises from a single cell that has accumulated multiple mutations
414(1)
Exposure to chemicals, radiation, and viruses can facilitate the progression to cancer
415(2)
The immune system is insensitive to emerging cancer
417(1)
Allogeneic bone marrow transplantation is the preferred treatment for many cancer patients
417(1)
Patients receiving an HLA-identical bone marrow transplant can still get GVHD
418(2)
Some GVHD helps engraftment and prevents relapse of malignant disease
420(1)
NK cells can also mediate GVL effects
420(1)
Cancer cells continue to acquire mutations throughout the cancer's lifetime
421(2)
Vaccination with tumor antigens can produce regression of cancer
423(2)
Tumors frequently evade immunity by downregulation of HLA class I
425(1)
Heat-shock proteins can provide natural adjuvants of tumor immunity
426(1)
Vaccination against oncogenic viruses
427(1)
Monoclonal antibodies against cell-surface tumor antigens can be used for diagnosis and immunotherapy
428(2)
Summary
429(1)
Summary to Chapter 12
429(1)
Questions
430


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