The Immune System

by Parham, P.

• ISBN13: 9780815340935
• ISBN10: 0815340931
• Edition: 2nd
• Format: Paperback
• Copyright: 2004-05-25
• Publisher: ROUTLEDGE

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