Book , Print in English

Janeway's immunobiology

Kenneth Murphy ; with acknowledgment to Charles A. Janeway, Jr., Paul Travers, Mark Walport ; with contributions by Allan Mowat, Casey T. Weaver.
  • New York : Garland Science, ©2012.
  • 8th ed.
  • xix, 868 pages : illustrations(chiefly colored) ; 28 cm.
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Subjects
Medical Subjects
Contents
  • pt. I INTRODUCTION TO IMMUNO- BIOLOGY AND INNATE IMMUNITY
  • ch. 1 Basic Concepts in Immunology
  • Principles of innate and adaptive immunity
  • 1-1. immune system recognizes infection and induces protective responses
  • 1-2. cells of the immune system derive from precursors in the bone marrow
  • 1-3. myeloid lineage comprises most of the cells of the innate immune system
  • 1-4. lymphoid lineage comprises the lymphocytes of the adaptive immune system and the natural killer cells of innate immunity
  • 1-5. Lymphocytes mature in the bone marrow or the thymus and then congregate in lymphoid tissues throughout the body
  • 1-6. Most infectious agents activate the innate immune system and induce an inflammatory response
  • 1-7. Pattern recognition receptors of the innate immune system provide an initial discrimination between self and nonself
  • 1-8. Adaptive immune responses are initiated by antigen and antigen-presenting cells in secondary lymphoid tissues
  • 1-9. Lymphocytes activated by antigen give rise to clones of antigen-specific effector cells that mediate adaptive immunity
  • 1-10. Clonal selection of lymphocytes is the central principle of adaptive immunity
  • 1-11. structure of the antibody molecule illustrates the central puzzle of adaptive immunity
  • 1-12. Each developing lymphocyte generates a unique antigen receptor by rearranging its receptor gene segments
  • 1-13. Immunoglobulins bind a wide variety of chemical structures, whereas the T-cell receptor is specialized to recognize foreign antigens as peptide fragments bound to proteins of the major histocompatibility complex
  • 1-14. development and survival of lymphocytes is determined by signals received through their antigen receptors
  • 1-15. Lymphocytes encounter and respond to antigen in the peripheral lymphoid organs
  • 1-16. Lymphocyte activation requires additional signals beyond those relayed from the antigen receptor when antigen binds
  • 1-17. Lymphocytes activated by antigen proliferate in the peripheral lymphoid organs, generating effector cells and immunological memory
  • Summary
  • effector mechanisms of adaptive immunity
  • 1-18. Antibodies protect against extracellular pathogens and their toxic products
  • 1-19. T cells orchestrate cell-mediated immunity and regulate B-cell responses to most antigens
  • 1-20. CD4 and CD8 T cells recognize peptides bound to two different classes of MHC molecules
  • 1-21. Inherited and acquired defects in the immune system result in increased susceptibility to infection
  • 1-22. Understanding adaptive immune responses is important for the control of allergies, autoimmune disease, and the rejection of transplanted organs
  • 1-23. Vaccination is the most effective means of controlling infectious diseases
  • Summary
  • Summary to Chapter 1
  • General references
  • ch. 2 Innate lmmunity: The First Lines of Defense
  • first lines of defense
  • 2-1. Infectious diseases are caused by diverse living agents that replicate in their hosts
  • 2-2. Infectious agents must overcome innate host defenses to establish a focus of infection
  • 2-3. Epithelial surfaces of the body provide the first line of defense against infection
  • 2-4. Epithelial cells and phagocytes produce several kinds of antimicrobial proteins
  • Summary
  • complement system and innate immunity
  • 2-5. complement system recognizes features of microbial surfaces and marks them for destruction by the deposition of C3b
  • 2-6. lectin pathway uses soluble receptors that recognize microbial surfaces to activate the complement cascade
  • 2-7. classical pathway is initiated by activation of the C1 complex and is homologous to the lectin pathway
  • 2-8. Complement activation is largely confined to the surface on which it is initiated
  • 2-9. alternative pathway is an amplification loop for C3b formation that is accelerated by recognition of pathogens by properdin
  • 2-10. Membrane and plasma proteins that regulate the formation and stability of C3 convertases determine the extent of complement activation under different circumstances
  • 2-11. Complement developed early in the evolution of multicellular organisms
  • 2-12. Surface-bound C3 convertase deposits large numbers of C3b fragments on pathogen surfaces and generates C5 convertase activity
  • 2-13. Ingestion of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins
  • 2-14. small fragments of some complement proteins initiate a local inflammatory response
  • 2-15. terminal complement proteins polymerize to form pores in membranes that can kill certain pathogens
  • 2-16. Complement control proteins regulate all three pathways of complement activation and protect the host from their destructive effects
  • Summary
  • Questions
  • Section references
  • ch. 3 Induced Responses of Innate Immunity
  • Pattern recognition by cells of the innate immune system
  • 3-1. After entering tissues, many pathogens are recognized, ingested, and killed by phagocytes
  • 3-2. G-protein-coupled receptors on phagocytes link microbe recognition with increased efficiency of intracellular killing
  • 3-3. Pathogen recognition and tissue damage initiate an inflammatory response
  • 3-4. Toll-like receptors represent an ancient pathogen-recognition system
  • 3-5. Mammalian Toll-like receptors are activated by many different pathogen-associated molecular patterns
  • 3-6. TLR-4 recognizes bacterial lipopolysaccharide in association with the host accessory proteins MD-2 and CD14
  • 3-7. TLRs activate the transcription factors NFkB, AP-1, and IRF to induce the expression of inflammatory cytokines and type I interferons
  • 3-8. NOD-like receptors act as intracellular sensors of bacterial infection
  • 3-9. RIG-l-like helicases detect cytoplasmic viral RNAs and stimulate interferon production
  • 3-10. Activation of TLRs and NLRs triggers changes in gene expression in macrophages and dendritic cells that have far-reaching effects on the immune response
  • 3-11. TLR signaling shares many components with Toll signaling in Drosophila
  • 3-12. TLR and NOD genes have undergone extensive diversification in both invertebrates and some primitive chordates
  • Summary
  • Induced innate responses to infection
  • 3-13. Macrophages and dendritic cells activated by pathogens secrete a range of cytokines that have a variety of local and distant effects
  • 3-14. Chemokines released by macrophages and dendritic cells recruit effector cells to sites of infection
  • 3-15. Cell-adhesion molecules control interactions between leukocytes and endothelial cells during an inflammatory response
  • 3-16. Neutrophils make up the first wave of cells that cross the blood vessel wall to enter an inflamed tissue
  • 3-17. TNF-α is an important cytokine that triggers local containment of infection but induces shock when released systemically
  • 3-18. Cytokines released by macrophages and dendritic cells activate the acute-phase response
  • 3-19. Interferons induced by viral infection make several contributions to host defense
  • 3-20. NK cells are activated by interferon and macrophage-derived cytokines to serve as an early defense against certain intracellular infections
  • 3-21. NK cells possess receptors for self molecules that prevent their activation by uninfected cells
  • 3-22. NK cells bear receptors that activate their effector function in response to ligands expressed on infected cells or tumor cells
  • 3-23. NKG2D receptor activates a different signaling pathway from that of the other activating NK receptors
  • 3-24. Several lymphocyte subpopulations behave as innate-like lymphocytes
  • Summary
  • Summary to Chapter 3
  • Questions
  • General references
  • Section references
  • pt. II RECOGNITION OF ANTIGEN
  • ch. 4 Antigen Recognition by B-cell and T-cell Receptors
  • structure of a typical antibody molecule
  • 4-1. IgG antibodies consist of four polypeptide chains
  • 4-2. Immunoglobulin heavy and light chains are composed of constant and variable regions
  • 4-3. antibody molecule can readily be cleaved into functionally distinct fragments
  • 4-4. immunoglobulin molecule is flexible, especially at the hinge region
  • 4-5. domains of an immunoglobulin molecule have similar structures
  • Summary
  • interaction of the antibody molecule with specific antigen
  • 4-6. Localized regions of hypervariable sequence form the antigen-binding site
  • 4-7. Antibodies bind antigens via contacts with amino acids in CDRs, but the details of binding depend upon the size and shape of the antigen
  • 4-8. Antibodies bind to conformational shapes on the surfaces of antigens
  • 4-9. Antigen-antibody interactions involve a variety of forces
  • Summary
  • Antigen recognition by T cells
  • 4-10. T-cell receptor is very similar to a Fab fragment of immunoglobulin
  • 4-11. T-cell receptor recognizes antigen in the form of a complex of a foreign peptide bound to an MHC molecule
  • 4-12. There are two classes of MHC molecules with distinct subunit compositions but similar three-dimensional structures
  • 4-13. Peptides are stably bound to MHC molecules, and also serve to stabilize the MHC molecule on the cell surface
  • 4-14. MHC class I molecules bind short peptides of 8--10 amino acids by both ends
  • 4-15. length of the peptides bound by MHC class II molecules is not constrained
  • 4-16. crystal structures of several peptide: MHC: T-cell receptor complexes show a similar orientation of the T-cell receptor over the peptide: MHC complex
  • 4-17. CD4 and CD8 cell-surface proteins of T cells are required to make an effective response to antigen --
  • Contents note continued: 4-18. two classes of MHC molecules are expressed differentially on cells
  • 4-19. distinct subset of T cells bears an alternative receptor made up of γ and δ chains
  • Summary
  • Summary to Chapter 4
  • Questions
  • General references
  • Section references
  • ch. 5 Generation of Lymphocyte Antigen Receptors
  • Primary immunoglobulin gene rearrangement
  • 5-1. Immunoglobulin genes are rearranged in antibody- producing cells
  • 5-2. Complete genes that encode a variable region are generated by the somatic recombination of separate gene segments
  • 5-3. Multiple contiguous V gene segments are present at each immunoglobulin locus
  • 5-4. Rearrangement of V, D, and J gene segments is guided by flanking DNA sequences
  • 5-5. reaction that recombines V, D, and J gene segments involves both lymphocyte-specific and ubiquitous DNA-modifying enzymes
  • 5-6. diversity of the immunoglobulin repertoire is generated by four main processes
  • 5-7. multiple inherited gene segments are used in different combinations
  • 5-8. Variable addition and subtraction of nucleotides at the junctions between gene segments contributes to the diversity of the third hypervariable region
  • Summary
  • T-cell receptor gene rearrangment
  • 5-9. T-cell receptor gene segments are arranged in a similar pattern to immunoglobulin gene segments and are rearranged by the same enzymes
  • 5-10. T-cell receptors concentrate diversity in the third hypervariable region
  • 5-11. γδ T-cell receptors are also generated by gene rearrangement
  • Summary
  • Structural variation in immunoglobulin constant regions
  • 5-12. Different classes of immunoglobulins are distinguished by the structure of their heavy-chain constant regions
  • 5-13. constant region confers functional specialization on the antibody
  • 5-14. Mature naive B cells express both IgM and IgD at their surface
  • 5-15. Transmembrane and secreted forms of immunoglobulin are generated from alternative heavy-chain transcripts
  • 5-16. IgM and IgA can form polymers
  • Summary
  • Secondary diversification of the antibody repertoire
  • 5-17. Activation-induced cytidine deaminase (AID) introduces mutations into genes transcribed in B cells
  • 5-18. Somatic hypermutation further diversifies the rearranged V regions of immunoglobulin genes
  • 5-19. Class switching enables the same assembled VHexon to be associated with different CHgenes in the course of an immune response
  • Summary
  • Evolution of the adaptive immune response
  • 5-20. Some invertebrates generate extensive diversity in a repertoire of immunoglobulin-like genes
  • 5-21. Agnathans possess an adaptive immune system that uses somatic gene rearrangement to diversify receptors built from LRR domains
  • 5-22. RAG-dependent adaptive immunity based on a diversified repertoire of immunoglobulin-like genes appeared abruptly in the cartilaginous fishes
  • 5-23. Different species generate immunoglobulin diversity in different ways
  • 5-24. Both α:β and γ:δ T-cell receptors are present in cartilaginous fish
  • 5-25. MHC class I and class II molecules are also first found in the cartilaginous fishes
  • Summary
  • Summary to Chapter 5
  • Questions
  • General references
  • Section references
  • ch. 6 Antigen Presentation to T Lymphocytes
  • Generation of T-cell receptor ligands
  • 6-1. MHC class I and class II molecules deliver peptides to the cell surface from two intracellular compartments
  • 6-2. Peptides that bind to MHC class I molecules are actively transported from the cytosol to the endoplasmic reticulum
  • 6-3. Peptides for transport into the endoplasmic reticulum are generated in the cytosol
  • 6-4. Newly synthesized MHC class I molecules are retained in the endoplasmic reticulum until they bind a peptide
  • 6-5. Many viruses produce immunoevasins that interfere with antigen presentation by MHC class I molecules
  • 6-6. Peptides presented by MHC class II molecules are generated in acidified endocytic vesicles
  • 6-7. invariant chain directs newly synthesized MHC class II molecules to acidified intracellular vesicles
  • 6-8. specialized MHC class ll-like molecule catalyzes loading of MHC class II molecules with peptides
  • 6-9. Cross-presentation allows exogenous proteins to be presented on MHC class I molecules by a restricted set of antigen-presenting cells
  • 6-10. Stable binding of peptides by MHC molecules provides effective antigen presentation at the cell surface
  • Summary
  • major histocompatibility complex and its function
  • 6-11. Many proteins involved in antigen processing and presentation are encoded by genes within the MHC
  • 6-12. protein products of MHC class I and class II genes are highly polymorphic
  • 6-13. MHC polymorphism affects antigen recognition by T cells by influencing both peptide binding and the contacts between T-cell receptor and MHC molecule
  • 6-14. Alloreactive T cells recognizing nonself MHC molecules are very abundant
  • 6-15. Many T cells respond to superantigens
  • 6-16. MHC polymorphism extends the range of antigens to which the immune system can respond
  • 6-17. variety of genes with specialized functions in immunity are also encoded in the MHC
  • 6-18. Specialized MHC class I molecules act as ligands for the activation and inhibition of NK cells
  • 6-19. CD1 family of MHC class Hike molecules is encoded outside the MHC and presents microbial lipids to CD1-restricted T cells
  • Summary
  • Summary to Chapter 6
  • Questions
  • General references
  • Section references
  • pt. III DEVELOPMENT OF MATURE LYMPHOCYTE RECEPTOR REPERTOIRES
  • ch. 7 Signaling Through Immune-System Receptors
  • General principles of signal transduction and propagation
  • 7-1. Transmembrane receptors convert extracellular signals into intracellular biochemical events
  • 7-2. Intracellular signal propagation is mediated by large multiprotein signaling complexes
  • 7-3. Small G proteins act as molecular switches in many different signaling pathways
  • 7-4. Signaling proteins are recruited to the membrane by a variety of mechanisms
  • 7-5. Ubiquitin conjugation of proteins can both activate and inhibit signaling responses
  • 7-6. activation of some receptors generates small-molecule second messengers
  • Summary
  • Antigen receptor signaling and lymphocyte activation
  • 7-7. Antigen receptors consist of variable antigen-binding chains associated with invariant chains that carry out the signaling function of the receptor
  • 7-8. Antigen recognition by the T-cell receptor and its co-receptors leads to phosphorylation of ITAMs by Src-family kinases
  • 7-9. Phosphorylated ITAMs recruit and activate the tyrosine kinase ZAP-70, which phosphorylates scaffold proteins that recruit the phospholipase PLC-γ
  • 7-10. activation of PLC-γ requires a co-stimulatory signal
  • 7-11. Activated PLC-γ generates the second messengers diacylglycerol and inositol trisphosphate
  • 7-12. Ca2+ entry activates the transcription factor NFAT
  • 7-13. Ras activation stimulates the mitogen-activated protein kinase (MAPK) relay and induces expression of the transcription factor AP-1
  • 7-14. Protein kinase C activates the transcription factors NFκB and AP-1
  • 7-15. cell-surface protein CD28 is a co-stimulatory receptor for naive T cells
  • 7-16. logic of B-cell receptor signaling is similar to that of T-cell receptor signaling, but some of the signaling components are specific to B cells
  • 7-17. ITAMs are also found in other receptors on leukocytes that signal for cell activation
  • 7-18. Inhibitory receptors on lymphocytes help regulate immune responses
  • Summary
  • Other receptors and signaling pathways
  • 7-19. Cytokines and their receptors fall into distinct families of structurally related proteins
  • 7-20. Cytokine receptors of the hematopoietin family are associated with the JAK family of tyrosine kinases, which activate STAT transcription factors
  • 7-21. Cytokine signaling is terminated by a negative feedback mechanism
  • 7-22. receptors that induce apoptosis activate specialized intracellular proteases called caspases
  • 7-23. intrinsic pathway of apoptosis is mediated by the release of cytochrome c from mitochondria
  • Summary
  • Summary to Chapter 7
  • Questions
  • General references
  • Section references
  • ch. 8 Development and Survival of Lymphocytes
  • Development of B lymphocytes
  • 8-1. Lymphocytes derive from hematopoietic stem cells in the bone marrow
  • 8-2. B-cell development begins by rearrangement of the heavy-chain locus
  • 8-3. pre-B-cell receptor tests for successful production of a complete heavy chain and signals for the transition from the pro-B cell to pre-B cell stage
  • 8-4. Pre-B-cell receptor signaling inhibits further heavy-chain locus rearrangement and enforces allelic exclusion
  • 8-5. Pre-B cells rearrange the light-chain locus and express cell-surface immunoglobulin
  • 8-6. Immature B cells are tested for autoreactivity before they leave the bone marrow
  • Summary
  • development of T lymphocytes in the thymus
  • 8-7. T-cell progenitors originate in the bone marrow, but all the important events in their development occur in the thymus
  • 8-8. T-cell precursors proliferate extensively in the thymus, but most die there
  • 8-9. Successive stages in the development of thymocytes are marked by changes in cell-surface molecules
  • 8-10. Thymocytes at different developmental stages are found in distinct parts of the thymus
  • 8-11. T cells with α:β or γ:δ receptors arise from a common progenitor --
  • Contents note continued: 8-12. T cells expressing particular γ- and δ-chain V regions arise in an ordered sequence early in life
  • 8-13. Successful synthesis of a rearranged β chain allows the production of a pre-T-cell receptor that triggers cell proliferation and blocks further β-chain gene rearrangement
  • 8-14. T-cell α-chain genes undergo successive rearrangements until positive selection or cell death intervenes
  • Summary
  • Positive and negative selection of T cells
  • 8-15. MHC type of the thymic stroma selects a repertoire of mature T cells that can recognize foreign antigens presented by the same MHC type
  • 8-16. Only thymocytes whose receptors interact with self-peptide: self-MHC complexes can survive and mature
  • 8-17. Positive selection acts on a repertoire of T-cell receptors with inherent specificity for MHC molecules
  • 8-18. Positive selection coordinates the expression of CD4 or CD8 with the specificity of the T-cell receptor and the potential effector functions of the T cell
  • 8-19. Thymic cortical epithelial cells mediate positive selection of developing thymocytes
  • 8-20. T cells that react strongly with ubiquitous self antigens are deleted in the thymus
  • 8-21. Negative selection is driven most efficiently by bone marrow derived antigen-presenting cells
  • 8-22. specificity and/or the strength of signals for negative and positive selection must differ
  • Summary
  • Survival and maturation of lymphocytes in peripheral lymphoid tissues
  • 8-23. Different lymphocyte subsets are found in particular locations in peripheral lymphoid tissues
  • 8-24. development of peripheral lymphoid tissues is controlled by lymphoid tissue inducer cells and proteins of the tumor necrosis factor family
  • 8-25. homing of lymphocytes to specific regions of peripheral lymphoid tissues is mediated by chemokines
  • 8-26. Lymphocytes that encounter sufficient quantities of self antigens for the first time in the periphery are eliminated or Inactivated
  • 8-27. Immature B cells arriving in the spleen turn over rapidly and require cytokines and positive signals through the B-cell receptor for maturation and survival
  • 8-28. B-1 cells and marginal zone B cells are distinct B-cell subtypes with unique antigen receptor specificity
  • 8-29. T-cell homeostasis in the periphery is regulated by cytokines and self-MHC interactions
  • Summary
  • Summary to Chapter 8
  • Questions
  • General references
  • Section references
  • pt. IV ADAPTIVE IMMUNE RESPONSE
  • ch. 9 T Cell-Mediated Immunity
  • Entry of naiveT cells and antigen-presenting cells into peripheral lymphoid organs
  • 9-1. Naive T cells migrate through peripheral lymphoid tissues, sampling the peptide: MHC complexes on dendritic cell surfaces
  • 9-2. Lymphocyte entry into lymphoid tissues depends on chemokines and adhesion molecules
  • 9-3. Activation of integrins by chemokines is responsible for the entry of naive T cells into lymph nodes
  • 9-4. T-cell responses are initiated in peripheral lymphoid organs by activated dendritic cells
  • 9-5. Dendritic cells process antigens from a wide array of pathogens
  • 9-6. Pathogen-induced TLR signaling in immature dendritic cells induces their migration to lymphoid organs and enhances antigen processing
  • 9-7. Plasmacytoid dendritic cells produce abundant type I interferons and may act as helper cells for antigen presentation by conventional dendritic cells
  • 9-8. Macrophages are scavenger cells that can be induced by pathogens to present foreign antigens to naive T cells
  • 9-9. B cells are highly efficient at presenting antigens that bind to their surface immunoglobulin
  • Summary
  • Priming of naive T cells by pathogen-activated dendritic cells
  • 9-10. Cell-adhesion molecules mediate the initial interaction of naive T cells with antigen-presenting cells
  • 9-11. Antigen-presenting cells deliver three kinds of signals for the clonal expansion and differentiation of naive T cells
  • 9-12. CD28-dependent co-stimulation of activated T cells induces expression of the T-cell growth factor interleukin-2 and the high-affinity IL-2 receptor
  • 9-13. Signal 2 can be modified by additional co-stimulatory pathways
  • 9-14. Antigen recognition in the absence of co-stimulation leads to functional inactivation or clonal deletion of peripheral T cells
  • 9-15. Proliferating T cells differentiate into effector T cells that do not require co-stimulation to act
  • 9-16. CD8 T cells can be activated in different ways to become cytotoxic effector cells
  • 9-17. CD4 T cells differentiate into several subsets of functionally different effector cells
  • 9-18. Various forms of signal 3 induce the differentiation of naive CD4 T cells down distinct effector pathways
  • 9-19. Regulatory CD4 T cells are involved in controlling adaptive immune responses
  • Summary
  • General properties of effector T cells and their cytokines
  • 9-20. Effector T-cell interactions with target cells are initiated by antigen-nonspecific cell-adhesion molecules
  • 9-21. immunological synapse forms between effector T cells and their targets to regulate signaling and to direct the release of effector molecules
  • 9-22. effector functions of T cells are determined by the array of effector molecules that they produce
  • 9-23. Cytokines can act locally or at a distance
  • 9-24. T cells express several TNF-family cytokines as trimeric proteins that are usually associated with the cell surface
  • Summary
  • T cell-mediated cytotoxicity
  • 9-25. Cytotoxic T cells can induce target cells to undergo programmed cell death
  • 9-26. Cytotoxic effector proteins that trigger apoptosis are contained in the granules of CD8 cytotoxic T cells
  • 9-27. Cytotoxic T cells are selective and serial killers of targets expressing a specific antigen
  • 9-28. Cytotoxic T cells also act by releasing cytokines
  • Summary
  • Macrophage activation by TH1 cells
  • 9-29. TH1 cells have a central role in macrophage activation
  • 9-30. Activation of macrophages by TH1 cells promotes microbial killing and must be tightly regulated to avoid tissue damage
  • 9-31. TH1 cells coordinate the host response to intracellular pathogens
  • Summary
  • Summary to Chapter 9
  • Questions
  • General references
  • Section references
  • ch. 10 Humoral Immune Response
  • B-cell activation by helper T cells
  • 10-1. humoral immune response is initiated when B cells that bind antigen are signaled by helper T cells or by certain microbial antigens alone
  • 10-2. B-cell responses are enhanced by co-ligation of the B-cell receptor and B-cell co-receptor by antigen and complement fragments on microbial surfaces
  • 10-3. Helper T cells activate B cells that recognize the same antigen
  • 10-4. T cells make membrane-bound and secreted molecules that activate B cells
  • 10-5. B cells that encounter their antigens migrate toward the boundaries between B-cell and T-cell areas in secondary lymphoid tissues
  • 10-6. Antibody-secreting plasma cells differentiate from activated B cells
  • 10-7. second phase of a primary B-cell immune response occurs when activated B cells migrate into follicles and proliferate to form germinal centers
  • 10-8. Germinal center B cells undergo V-region somatic hypermutalion, and cells with mutations that improve affinity for antigen are selected
  • 10-9. Class switching in thymus-dependent antibody responses requires expression of CD40 ligand by helper T cells and is directed by cytokines
  • 10-10. Ligation of CD40 and prolonged contact with T follicular helper cells is required to sustain germinal center B cells
  • 10-11. Surviving germinal center B cells differentiate into either plasma cells or memory cells
  • 10-12. Some bacterial antigens do not require T-cell help to induce B-cell responses
  • 10-13. B-cell responses to bacterial polysaccharides do not require peptide-specific T-cell help
  • Summary
  • distributions and functions of immunoglobulin classes
  • 10-14. Antibodies of different classes operate in distinct places and have distinct effector functions
  • 10-15. Transport proteins that bind to the Fc regions of antibodies carry particular isotypes across epithelial barriers
  • 10-16. High-affinity IgG and IgA antibodies can neutralize bacterial toxins
  • 10-17. High-affinity IgG and IgA antibodies can inhibit the infectivity of viruses
  • 10-18. Antibodies can block the adherence of bacteria to host cells
  • 10-19. Antibody: antigen complexes activate the classical pathway of complement by binding to C1q
  • 10-20. Complement receptors are important in the removal of immune complexes from the circulation
  • Summary
  • destruction of antibody-coated pathogens via Fc receptors
  • 10-21. Fc receptors of accessory cells are signaling receptors specific for immunoglobulins of different classes
  • 10-22. Fc receptors on phagocytes are activated by antibodies bound to the surface of pathogens and enable the phagocytes to ingest and destroy pathogens
  • 10-23. Fc receptors activate NK cells to destroy antibody-coated targets
  • 10-24. Mast cells and basophils bind IgE antibody via the high-affinity Fee receptor
  • 10-25. IgE-mediated activation of accessory cells has an important role in resistance to parasite infection
  • Summary
  • Summary to Chapter 10
  • Questions
  • General references
  • Section references
  • ch. 11 Dynamics of Adaptive Immunity
  • course of the immune response to infection
  • 11-1. course of an infection can be divided into several distinct phases
  • 11-2. nonspecific responses of innate immunity are necessary for an adaptive immune response to be initiated --
  • Contents note continued: 11-3. Cytokines made during infection can direct differentiation of CD4T cells toward the TH17 subset
  • 11-4. TH1 and TH2 cells are induced by cytokines generated in response to different pathogens
  • 11-5. CD4 T-cell subsets can cross-regulate each other's differentiation
  • 11-6. Effector T cells are guided to sites of infection by chemokines and newly expressed adhesion molecules
  • 11-7. Differentiated effector T cells are not a static population but continue to respond to signals as they carry out their effector functions
  • 11-8. Primary CD8 T-cell responses to pathogens can occur in the absence of CD4 T-cell help
  • 11-9. Antibody responses develop in lymphoid tissues under the direction of TFHcells
  • 11-10. Antibody responses are sustained in medullary cords and bone marrow
  • 11-11. effector mechanisms used to clear an infection depend on the infectious agent
  • 11-12. Resolution of an infection is accompanied by the death of most of the effector cells and the generation of memory cells
  • Summary
  • Immunological memory
  • 11-13. Immunological memory is long-lived after infection or vaccination
  • 11-14. Memory B-cell responses differ in several ways from those of naive B cells
  • 11-15. Repeated immunization leads to increasing affinity of antibody due to somatic hypermutation and selection by antigen in germinal centers
  • 11-16. Memory T cells are increased in frequency compared with naive T cells specific for the same antigen, and have distinct activation requirements and cell-surface proteins that distinguish them from effector T cells
  • 11-17. Memory T cells are heterogeneous and include central memory and effector memory subsets
  • 11-18. CD4 T-cell help is required for CD8 T-cell memory and involves CD40 and IL-2 signaling
  • 11-19. In immune individuals, secondary and subsequent responses are mainly attributable to memory lymphocytes
  • Summary
  • Summary to Chapter 11
  • Questions
  • Section references
  • ch. 12 Mucosal Immune System
  • Organisation of the mucosal system
  • 12-1. mucosal immune system protects the internal surfaces of the body
  • 12-2. mucosal immune system may be the original vertebrate immune system
  • 12-3. Cells of the mucosal immune system are located both in anatomically defined compartments and scattered throughout mucosal tissues
  • 12-4. intestine has distinctive routes and mechanisms of antigen uptake
  • 12-5. mucosal immune system contains large numbers of effector lymphocytes even in the absence of disease
  • 12-6. circulation of lymphocytes within the mucosal immune system is controlled by tissue-specific adhesion molecules and chemokine receptors
  • 12-7. Priming of lymphocytes in one mucosal tissue can induce protective immunity at other mucosal surfaces
  • 12-8. Unique populations of dendritic cells controf mucosal immune responses
  • 12-9. intestinal lamina propria contains antigen-experienced T cells and populations of unusual innate-type lymphocytes
  • 12-10. intestinal epithelium is a unique compartment of the immune system
  • 12-11. Secretory IgA is the class of antibody associated with the mucosal immune system
  • 12-12. IgA deficiency is common in humans but may be compensated for by secretory IgM
  • Summary
  • mucosal response to infection and regulation of mucosal immune responses
  • 12-13. Enteric pathogens cause a local inflammatory response and the development of protective immunity
  • 12-14. outcome of infection by intestinal pathogens is determined by a complex interplay between the microorganism and the host immune response
  • 12-15. mucosal immune system must maintain a balance between protective immunity and homeostasis to a large number of different foreign antigens
  • 12-16. healthy intestine contains large quantities of bacteria but does not generate potentially harmful immune responses against them
  • 12-17. Full immune responses to commensal bacteria provoke intestinal disease
  • 12-18. Intestinal helminths provoke strong TH2-mediated immune responses
  • 12-19. Other eukaryotic parasites provoke protective immunity and pathology in the gut
  • 12-20. mucosal immune system has to compromise between suppression and activation of an immune response
  • Summary
  • Summary to Chapter 11
  • Questions
  • General references
  • Section references
  • pt. V IMMUNE SYSTEM IN HEALTH AND DISEASE
  • ch. 13 Failures of Host Defense Mechanisms
  • Evasion and subversion of immune defenses
  • 13-1. Antigenic variation allows pathogens to escape from immunity
  • 13-2. Some viruses persist in vivo by ceasing to replicate until immunity wanes
  • 13-3. Some pathogens resist destruction by host defense mechanisms or exploit them for their own purposes
  • 13-4. Immunosuppression or inappropriate immune responses can contribute to persistent disease
  • 13-5. Immune responses can contribute directly to pathogenesis
  • 13-6. Regulatory T cells can affect the outcome of infectious disease
  • Summary
  • Immunodeficiency diseases
  • 13-7. history of repeated infections suggests a diagnosis of immunodeficiency
  • 13-8. Primary immunodeficiency diseases are caused by inherited gene defects
  • 13-9. Defects in T-cell development can result in severe combined immunodeficiencies
  • 13-10. SCID can also be due to defects in the purine salvage pathway
  • 13-11. Defects in antigen receptor gene rearrangement can result in SCID
  • 13-12. Defects in signaling from T-cell antigen receptors can cause severe immunodeficiency
  • 13-13. Genetic defects in thymic function that block T-cell development result in severe immunodeficiencies
  • 13-14. Defects in B-cell development result in deficiencies in antibody production that cause an inability to clear extracellular bacteria
  • 13-15. Immune deficiencies can be caused by defects in B-cell or T-cell activation and function
  • 13-16. Defects in complement components and complement-regulatory proteins cause defective humoral immune function and tissue damage
  • 13-17. Defects in phagocytic cells permit widespread bacterial infections
  • 13-18. Mutation in the molecular regulators of inflammation can cause uncontrolled inflammatory responses that result in `autoinflammatory disease.'
  • 13-19. normal pathways for host defense against intracellular bacteria are pinpointed by genetic deficiencies of IFN-γ and IL-12 and their receptors
  • 13-20. X-linked lymphoproliferative syndrome is associated with fatal infection by Epstein-Barr virus and with the development of lymphomas
  • 13-21. Genetic abnormalities in the secretory cytotoxic pathway of lymphocytes cause uncontrolled lymphoproliferation and inflammatory responses to viral infections
  • 13-22. Hematopoietic stem cell transplantation or gene therapy can be useful to correct genetic defects
  • 13-23. Secondary immunodeficiencies are major predisposing causes of infection and death
  • Summary
  • Acquired immune deficiency syndrome
  • 13-24. Most individuals infected with HIV progress over time to AIDS
  • 13-25. HIV is a retrovirus that infects CD4 T cells, dendritic cells, and macrophages
  • 13-26. Genetic variation in the host can alter the rate of progression of disease
  • 13-27. genetic deficiency of the co-receptor CCR5 confers resistance to HIV infection in vivo
  • 13-28. HIV RNA is transcribed by viral reverse transcriptase into DNA that integrates into the host-cell genome
  • 13-29. Replication of HIV occurs only in activated T cells
  • 13-30. Lymphoid tissue is the major reservoir of HIV infection
  • 13-31. immune response controls but does not eliminate HIV
  • 13-32. destruction of immune function as a result of HIV infection leads to increased susceptibility to opportunistic infection and eventually to death
  • 13-33. Drugs that block HIV replication lead to a rapid decrease in titer of infectious virus and an increase in CD4 T cells
  • 13-34. HIV accumulates many mutations in the course of infection, and drug treatment is soon followed by the outgrowth of drug-resistant variants
  • 13-35. Vaccination against HIV is an attractive solution but poses many difficulties
  • 13-36. Prevention and education are one way in which the spread of HIV and AIDS can be controlled
  • Summary
  • Summary to Chapter 13
  • Questions
  • General references
  • Section references
  • ch. 14 Allergy and Allergic Diseases
  • IgE and IgE-mediated allergic diseases
  • 14-1. Sensitization involves class switching to IgE production on first contact with an allergen
  • 14-2. Allergens are usually delivered transmucosally at low dose, a route that favors IgE production
  • 14-3. Genetic factors contribute to the development of IgE- mediated allergic disease
  • 14-4. Environmental factors may interact with genetic susceptibility to cause allergic disease
  • 14-5. Regulatory T cells can control allergic responses
  • Summary
  • Effector mechanisms in IgE-mediated allergic reactions
  • 14-6. Most IgE is cell-bound and engages effector mechanisms of the immune system by different pathways from those of other antibody isotypes
  • 14-7. Mast cells reside in tissues and orchestrate allergic reactions
  • 14-8. Eosinophils and basophils cause inflammation and tissue damage in allergic reactions
  • 14-9. IgE-mediated allergic reactions have a rapid onset but can also lead to chronic responses
  • 14-10. Allergen introduced into the bloodstream can cause anaphylaxis
  • 14-11. Allergen inhalation is associated with the development of rhinitis and asthma
  • 14-12. genetically determined defect in the skin's barrier function increases the risk of atopic eczema
  • 14-13. Allergy to particular foods causes systemic reactions as well as symptoms limited to the gut --
  • Contents note continued: 14-14. IgE-mediated allergic disease can be treated by inhibiting the effector pathways that lead to symptoms or by desensitization techniques that aim at restoring tolerance to the allergen
  • Summary
  • Non-lgE-mediated allergic diseases
  • 14-15. Innocuous antigens can cause type II hypersensitivity reactions in susceptible individuals by binding to the surfaces of circulating blood cells
  • 14-16. Systemic disease caused by immune-complex formation can follow the administration of large quantities of poorly catabolized antigens
  • 14-17. Hypersensitivity reactions can be mediated by TH1 cells and CD8 cytotoxic T cells
  • 14-18. Celiac disease has features of both an allergic response and autoimmunity
  • Summary
  • Summary to Chapter 14
  • Questions
  • General references
  • Section references
  • ch. 15 Autoimmunity and Transplantation
  • making and breaking of self-tolerance
  • 15-1. critical function of the immune system is to discriminate self from nonself
  • 15-2. Multiple tolerance mechanisms normally prevent autoimmunity
  • 15-3. Central deletion or inactivation of newly formed lymphocytes is the first checkpoint of self-tolerance
  • 15-4. Lymphocytes that bind self antigens with relatively low affinity usually ignore them but in some circumstances become activated
  • 15-5. Antigens in immunologically privileged sites do not induce immune attack but can serve as targets
  • 15-6. Autoreactive T cells that express particular cytokines may be nonpathogenic or may suppress pathogenic lymphocytes
  • 15-7. Autoimmune responses can be controlled at various stages by regulatory T cells
  • Summary
  • Autoimmune diseases and pathogenic mechanisms
  • 15-8. Specific adaptive immune responses to self antigens can cause autoimmune disease
  • 15-9. Autoimmune diseases can be classified into clusters that are typically either organ-specific or systemic
  • 15-10. Multiple components of the immune system are typically recruited in autoimmune disease
  • 15-11. Chronic autoimmune disease develops through positive feedback from inflammation, inability to clear the self antigen, and a broadening of the autoimmune response
  • 15-12. Both antibody and effector T cells can cause tissue damage in autoimmune disease
  • 15-13. Autoantibodies against blood cells promote their destruction
  • 15-14. fixation of sublytic doses of complement to cells in tissues stimulates a powerful inflammatory response
  • 15-15. Autoantibodies against receptors cause disease by stimulating or blocking receptor function
  • 15-16. Autoantibodies against extracellular antigens cause inflammatory injury by mechanisms akin to type II and type III hypersensitivity reactions
  • 15-17. T cells specific for self antigens can cause direct tissue injury and sustain autoantibody responses
  • Summary
  • genetic and environmental basis of autoimmunity
  • 15-18. Autoimmune diseases have a strong genetic component
  • 15-19. Several approaches have given us insight into the genetic basis of autoimmunity
  • 15-20. Many genes that predispose to autoimmunity fall into categories that affect one or more of the mechanisms of tolerance
  • 15-21. defect in a single gene can cause autoimmune disease
  • 15-22. MHC genes have an important role in controlling susceptibility to autoimmune disease
  • 15-23. Genetic variants that impair innate immune responses can predispose to T cell-mediated chronic inflammatory disease
  • 15-24. External events can initiate autoimmunity
  • 15-25. Infection can lead to autoimmune disease by providing an environment that promotes lymphocyte activation
  • 15-26. Cross-reactivity between foreign molecules on pathogens and self molecules can lead to anti-self responses and autoimmune disease
  • 15-27. Drugs and toxins can cause autoimmune syndromes
  • 15-28. Random events may be required for the initiation of autoimmunity
  • Summary
  • Responses to alloantigens and transplant rejection
  • 15-29. Graft rejection is an immunological response mediated primarily by T cells
  • 15-30. Transplant rejection is caused primarily by the strong immune response to nonself MHC molecules
  • 15-31. In MHC-identical grafts, rejection is caused by peptides from other alloantigens bound to graft MHC molecules
  • 15-32. There are two ways of presenting alloantigens on the transplanted donor organ to the recipient's T lymphocytes
  • 15-33. Antibodies that react with endothelium cause hyperacute graft rejection
  • 15-34. Late failure of transplanted organs is caused by chronic injury to the graft
  • 15-35. variety of organs are transplanted routinely in clinical medicine
  • 15-36. converse of graft rejection is graft-versus-host disease
  • 15-37. Regulatory T cells are involved in alloreactive immune responses
  • 15-38. fetus is an allograft that is tolerated repeatedly
  • Summary
  • Summary to Chapter 15
  • Questions
  • Section references
  • ch. 16 Manipulation of the Immune Response
  • Treatment of unwanted immune responses
  • 16-1. Corticosteroids are powerful anti-inflammatory drugs that alter the transcription of many genes
  • 16-2. Cytotoxic drugs cause immunosuppression by killing dividing cells and have serious side-effects
  • 16-3. Cyclosporin A, tacrolimus (FK506), and rapamycin (sirolimus) are powerful immunosuppressive agents that interfere with T-cell signaling
  • 16-4. Antibodies against cell-surface molecules can be used to eliminate lymphocyte subsets or to inhibit lymphocyte function
  • 16-5. Antibodies can be engineered to reduce their immunogenicity in humans
  • 16-6. Monoclonal antibodies can be used to prevent allograft rejection
  • 16-7. Depletion of autoreactive lymphocytes can treat autoimmune disease
  • 16-8. Biologic agents that block TNF-α or IL-1 can alleviate autoimmune diseases
  • 16-9. Biologic agents can block cell migration to sites of inflammation and reduce immune responses
  • 16-10. Blockade of co-stimulatory pathways that activate lymphocytes can be used to treat autoimmune disease
  • 16-11. Some commonly used drugs have immunomodulatory properties
  • 16-12. Controlled administration of antigen can be used to manipulate the nature of an antigen-specific response
  • Summary
  • Using the immune response to attack tumors
  • 16-13. development of transplantable tumors in mice led to the discovery ot protective immune responses to tumors
  • 16-14. Tumors are `edited' by the immune system as they evolve and can escape rejection in many ways
  • 16-15. Tumor-specific antigens can be recognized by T cells and form the basis of immunotherapies
  • 16-16. Monoclonal antibodies against tumor antigens, alone or linked to toxins, can control tumor growth
  • 16-17. Enhancing the immune response to tumors by vaccination holds promise for cancer prevention and therapy
  • 16-18. Checkpoint blockade can augment immune responses to existing tumors
  • Summary
  • Fighting infectious diseases with vaccination
  • 16-19. Vaccines can be based on attenuated pathogens or material from killed organisms
  • 16-20. Most effective vaccines generate antibodies that prevent the damage caused by toxins or that neutralize the pathogen and stop infection
  • 16-21. Effective vaccines must induce long-lasting protection while being safe and inexpensive
  • 16-22. Live-attenuated viral vaccines are usually more potent than `killed' vaccines and can be made safer by the use of recombinant DNA technology
  • 16-23. Live-attenuated vaccines can be developed by selecting nonpathogenic or disabled bacteria or by creating genetically attenuated parasites (GAPs)
  • 16-24. route of vaccination is an important determinant of success
  • 16-25. Bordetella pertussis vaccination illustrates the Importance of the perceived safety of a vaccine
  • 16-26. Conjugate vaccines have been developed as a result of understanding how T and B cells collaborate in an immune response
  • 16-27. Peptide-based vaccines can elicit protective immunity, but they require adjuvants and must be targeted to the appropriate cells and cell compartment to be effective
  • 16-28. Adjuvants are important for enhancing the immunogenicity of vaccines, but few are approved for use in humans
  • 16-29. Protective immunity can be induced by DNA-based vaccination
  • 16-30. effectiveness of a vaccine can be enhanced by targeting it to sites of antigen presentation
  • 16-31. important question is whether vaccination can be used therapeutically to control existing chronic infections
  • Summary
  • Summary to Chapter 16
  • Questions
  • General references
  • Section references
  • Appendix I Immunologist's Toolbox
  • Immunization
  • A-1. Haptens
  • A-2. Routes of immunization
  • A-3. Effects of antigen dose
  • A-4. Adjuvants
  • detection, measurement, and characterization of antibodies and their use as research and diagnostic tools
  • A-5. Affinity chromatography
  • A-6. Radioimmunoassay (RIA), enzyme-linked immunosorbent assay (ELISA), and competitive inhibition assay
  • A-7. Hemagglutination and blood typing
  • A-8. Precipitin reaction
  • A-9. Equilibrium dialysis: measurement of antibody affinity and avidity
  • A-10. Anti-immunoglobulin antibodies
  • A-11. Coombs tests and the detection of Rhesus incompatibility
  • A-12. Monoclonal antibodies
  • A-13. Phage display libraries for antibody V-region production
  • A-14. Microscopy and imaging
  • A-15. Immunoelectron microscopy
  • A-16. Immunohistochemistry
  • A-17. Immunoprecipitation and co-immunoprecipitation
  • A-18. Immunoblotting (Western blotting)
  • A-19. Use of antibodies in the isolation and identification of genes and their products
  • Isolation of lymphocytes --
  • Contents note continued: A-20. Isolation of peripheral blood lymphocytes by Ficoll-Hypaque[™] gradient
  • A-21. Isolation of lymphocytes from tissues other than blood
  • A-22. Flow cytometry and FACS analysis
  • A-23. Lymphocyte isolation using antibody-coated magnetic beads
  • A-24. Isolation of homogeneous T-cell lines
  • Characterization of lymphocyte specificity, frequency, and function
  • A-25. Limiting-dilution culture
  • A-26. EL1SPOT assays
  • A-27. Identification of functional subsets of T cells by staining for cytokines
  • A-28. Identification of T-cell receptor specificity using peptide: MHC tetramers
  • A-29. Assessing the diversity of the T-cell repertoire by `spectratyping.'
  • A-30. Biosensor assays for measuring the rates of association and disassociation of antigen receptors for their ligands
  • A-31. Stimulation of lymphocyte proliferation by treatment with polyclonal mitogens or specific antigen
  • A-32. Measurements of apoptosis by the TUNEL assay
  • A-33. Assays for cytotoxic T cells
  • A-34. Assays for CD4 T cells
  • Detection of immunity in vivo
  • A-35. Assessment of protective immunity
  • A-36. Transfer of protective immunity
  • A-37. tuberculin test
  • A-38. Testing for allergic responses
  • A-39. Assessment of immune responses and immunological competence in humans
  • A-40. Arthus reaction
  • A-41. Adoptive transfer of lymphocytes
  • A-42. Hematopoietic stem-cell transfers
  • A-43. In vivo depletion of T cells
  • A-44. In vivo depletion of B cells
  • A-45. Transgenic mice
  • A-46. Gene knockout by targeted disruption
  • Appendix II CD Antigens
  • Appendix III Cytokines and Their Receptors
  • Appendix IV Chemokines and Their Receptors.
Other information
  • Prev. ed. 2008.
  • Includes bibliographical references and index.
ISBN
  • 9780815342434 (alk. paper)
  • 0815342438 (alk. paper)
Identifying numbers
  • LCCN: 2011023486
  • OCLC: 733935898

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