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Summary Table of Contents Author Biography

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.

Elements of the Immune System and their Roles in Defense

(36)

Defenses facing invading pathogens

(1)

Pathogens are inf... MORE

(3)

The skin and mucosal surfaces form physical barriers against infection

(2)

The innate immune response causes inflammation at sites of infection

(1)

The adaptive immune response adds to an ongoing innate immune response

(3)

Immune system cells with different functions all derive from hematopoietic stem cells

(4)

Most lymphocytes are present in specialized lymphoid tissues

(1)

Lymphocytes are activated in the secondary lymphoid tissues

(5)

Summary

(1)

Principles of adaptive immunity

(1)

Immunoglobulins and T-cell receptors are the highly variable recognition molecules of adaptive immunity

(1)

The diversity of immunoglobulins and T-cell receptors is generated by gene rearrangement

(1)

B cells recognize intact pathogens, whereas T cells recognize pathogen-derived peptides bound to proteins of the major histocompatibility complex

(1)

Clonal selection of B and T lymphocytes is the guiding principle of the adaptive immune response

(2)

Extracellular pathogens and their toxins are eliminated by antibodies

(2)

Adaptive immune responses generally give rise to long-lived immunological memory and protective immunity

(1)

The immune system can be compromised by inherited immunodeficiencies or by the actions of certain pathogens

(1)

Unwanted effects of adaptive immunity cause allergy, autoimmune disease, and rejection of transplanted tissues

(7)

Summary

(1)

Summary to Chapter 1

(1)

Questions

(3)

Antibody Structure and the Generation of B-Cell Diversity

(30)

The structural basis of antibody diversity

(1)

Antibodies are composed of polypeptides with variable and constant regions

(2)

Immunoglobulin chains are folded into compact and stable protein domains

(1)

An antigen-binding site is formed from the hypervariable regions of a heavy-chain and a light-chain V domain

(1)

Antigen-binding sites vary in shape and physical properties

(3)

Monoclonal antibodies are produced from a clone of antibody-producing cells

(3)

Summary

(1)

Generation of immunoglobulin diversity in B cells before encounter with antigen

(1)

The DNA sequence encoding a V region is assembled from two or three gene segments

(1)

Random recombination of gene segments produces diversity in the antigen-binding sites of immunoglobulins

(2)

Recombination enzymes produce additional diversity in the antigen-binding sites of immunoglobulins

(1)

Naive B cells use alternative mRNA splicing to make both IgM and IgD

(1)

Each B cell produces immunoglobulin of a single antigen specificity

(2)

Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface

(1)

Summary

(1)

Diversification of antibodies after B cells encounter antigen

(1)

Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing

(1)

Rearranged V-region sequences are further diversified by somatic hypermutation

(1)

Isotype switching produces immunoglobulins with different C regions but identical antigen specificities

(1)

Antibodies with different C regions have different effector functions

(9)

Summary

(1)

Summary to Chapter 2

(2)

Questions

(4)

Antigen Recognition by T Lymphocytes

(32)

T-cell receptor diversity

(1)

The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin

(1)

T-cell receptor diversity is generated by gene rearrangement

(2)

Expression of the T-cell receptor on the cell surface requires association with additional proteins

(1)

γ and δ chains form a second class of T-cell receptor expressed by a distinct population of T cells

(3)

Summary

(1)

Antigen processing and presentation

(1)

Two classes of T cell are specialized to respond to intracellular and extracellular sources of infection

(1)

Two classes of MHC molecule present antigen to CD8 and CD4 T cells respectively

(1)

The two classes of MHC molecule have similar three-dimensional structures

(1)

MHC molecules bind a variety of peptides

(1)

Peptides generated in the cytosol are transported into the endoplasmic reticulum where they bind MHC class I molecules

(2)

Peptides presented by MHC class II molecules are generated in acidified intracellular vesicles

(2)

MHC class II molecules are prevented from binding peptides in the endoplasmic reticulum by the invariant chain

(1)

The T-cell receptor specifically recognizes both peptide and MHC molecule

(1)

The two classes of MHC molecule are expressed differentially on cells

(3)

Summary

(1)

The major histocompatibility complex

(1)

The diversity of MHC molecules in the human population is due to multigene families and genetic polymorphism

(1)

The MHC class I and class II genes occupy different regions of the MHC

(1)

Other proteins involved in antigen processing and presentation are encoded in the MHC class II region

(1)

MHC polymorphism affects the binding and presentation of peptide antigens to T cells

(1)

MHC diversity results from selection by infectious disease

(3)

MHC polymorphism triggers T-cell reactions that can reject transplanted organs

(6)

Summary

(1)

Summary to Chapter 3

(1)

Questions

(4)

The Development of B Lymphocytes

(12)

The development of B cells in the bone marrow

(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

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

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The Immune System

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