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Book Cover
Author Parham, Peter, 1950- author

Title The immune system / Peter Parham
Edition Fifth edition
International student edition
Published New York, NY : W.W. Norton & Company, [2021]


Location Call no. Vol. Availability
 W'PONDS  616.079 Par/Isy 2021  AVAILABLE
Description xxv, 529, 12, 34, 4, 20 pages : illustrations (some color) ; 28 cm
Contents Machine generated contents note: ch. 1 Elements of the Immune System and Their Roles in Defense -- 1-1.Numerous commensal microorganisms inhabit healthy human bodies -- 1-2.Pathogens are infectious organisms that cause disease -- 1-3.Skin and mucosal surfaces are barrier defenses against infection -- 1-4.The innate immune response produces a state of inflammation at sites of infection -- 1-5.The adaptive immune response builds on the innate immune response -- 1-6.Immune-system cells with different functions derive from hematopoietic stem cells -- 1-7.Immunoglobulins and T-cell receptors are the antigen receptors of adaptive immunity -- 1-8.On binding specific antigen, B cells and T cells divide and differentiate into effector cells -- 1-9.B cells and T cells recognize different categories of microbial antigens -- 1-10.Antibodies binding to a pathogen cause its inactivation or elimination -- 1-11.Most lymphocytes are present in specialized lymphoid tissues -- 1-12.Adaptive immunity is initiated in secondary lymphoid tissues -- 1-13.The spleen provides adaptive immunity to blood infections -- 1-14.Most of the body's secondary lymphoid tissue is associated with the gut -- Summary to Chapter 1 -- Questions -- ch. 2 Innate Immunity: the Immediate Response to Infection -- 2-1.Physical barriers colonized by commensal microorganisms protect against infection by pathogens -- 2-2.Different immune responses are targeted to extracellular and intracellular infections -- 2-3.Complement is a system of plasma proteins that mark pathogens for destruction -- 2-4.At the start of an infection, complement activation proceeds by the alternative pathway -- 2-5.Regulatory proteins determine the extent and site of C3b deposition -- 2-6.The macrophage is a first line of cellular defense against an invading microorganism -- 2-7.The terminal complement components make pores in microbial membranes -- 2-8.Small peptides released during complement activation induce local inflammation -- 2-9.Several systems of plasma proteins limit the spread of infection -- 2-10.Defensins are antimicrobial peptides that kill pathogens by disrupting their membranes -- 2-11.Pentraxins are plasma proteins that bind microorganisms and deliver them to phagocytes -- Summary to Chapter 2 -- Questions -- ch. 3 Innate Immunity: the Induced Response to Infection -- Inflammation, innate immunity, and myeloid cells -- 3-1.The receptors of innate immunity distinguish ̀self' from ̀non-self' and ̀altered-self' -- 3-2.Tissue-resident macrophages use a multiplicity of surface receptors to detect infection -- 3-3.Toll-like receptor 4 recognizes the lipopolysaccharide of Gram-negative bacteria -- 3-4.Toll-like receptors sense the presence of the four main groups of pathogenic microorganisms -- 3-5.TLR4 polymorphism influences disease susceptibility -- 3-6.Intracellular NOD proteins recognize bacterial degradation products in the cytoplasm -- 3-7.Cells infected with a virus make an interferon response -- 3-8.Plasmacytoid dendritic cells specialize in the production of type I interferons -- 3-9.Inflammasomes enable activated macrophages to release a large burst of IL-1[beta] -- 3-10.IL-[alpha] and IL-1[beta] are members of a diverse and highly conserved cytokine family -- 3-11.Autoinflammatory diseases arise from innate immune responses that attack self -- 3-12.Inflammation of an infected tissue attracts blood-borne immune effector cells -- 3-13.Recruitment of neutrophils from blood to tissue is mediated by adhesion molecules -- 3-14.Neutrophils are potent killers of pathogens and are programmed to die -- 3-15.Inflammatory cytokines cause fever and induce the acute-phase response by the liver -- 3-16.The lectin pathway of complement activation is initiated by the mannose-binding lectin -- 3-17.C-reactive protein triggers the classical pathway of complement activation -- Summary -- Inflammation, innate immunity, and lymphoid cells -- 3-18.Five types of innate lymphoid cell contribute to inflammation and innate immunity -- 3-19.The five types of innate lymphoid cell derive from a common innate lymphocyte precursor -- 3-20.NK cells are circulating lymphocytes of the innate immune response -- 3-21.Two subpopulations of NK cells are differentially distributed in blood and tissues -- 3-22.NK-cell cytotoxicity is activated at sites of virus infection -- 3-23.NK cells and macrophages activate each other at sites of infection -- 3-24.Interactions between dendritic cells and NK cells influence the immune response -- 3-25.The NK-cell population retains a memory of its encounters with pathogens -- Summary -- Summary to Chapter 3 -- Questions -- ch. 4 Antibody Structure and the Generation of B-Cell Diversity -- The structural basis of antibody diversity -- 4-1.Antibodies are composed of polypeptides with variable and constant regions -- 4-2.Immunoglobulin chains are folded into compact and stable protein domains -- 4-3.The antigen-binding site of an antibody is formed from the hypervariable regions of the heavy- and light-chain V domains -- 4-4.Antigen-binding sites vary in shape and physical properties -- 4-5.A monoclonal antibody is produced by a clone of antibody-producing cells -- 4-6.Monoclonal antibodies are used as treatments for a variety of diseases -- Summary -- Generation of immunoglobulin diversity in B cells before encounter with antigen -- 4-7.The DNA sequence encoding a V region is assembled from two or three gene segments -- 4-8.Random recombination of gene segments creates diversity in the antigen-binding sites of immunoglobulins -- 4-9.Recombination enzymes produce additional diversity in the antigen-binding site -- 4-10.In naive B cells alternative mRNA splicing produces IgM and IgD of the same antigen specificity -- 4-11.Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface -- Summary -- Diversification of antibodies after B cells encounter antigen -- 4-12.Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing -- 4-13.Rearranged V-region sequences are further diversified by somatic hypermutation -- 4-14.Isotype switching produces immunoglobulin with a different constant region but identical antigen specificity -- 4-15.Antibodies with different constant regions have different effector functions -- 4-16.The four subclasses of IgG have different and complementary functions -- Summary -- Summary to Chapter 4 -- Questions -- ch. 5 Antigen Recognition by T Lymphocytes -- T-cell receptor diversity -- 5-1.The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin -- 5-2.T-cell receptor diversity is generated by gene rearrangement -- 5-3.Expression of the T-cell receptor on the T-cell surface requires association with additional proteins -- 5-4.A distinctive population of T cells expresses a second class of T-cell receptor with [gamma] and [delta] chains -- Summary -- Antigen processing and presentation -- 5-5.T-cell receptors recognize peptide antigens bound to MHC molecules -- 5-6.Two classes of MHC molecule present peptide antigens to two types of T cell -- 5-7.MHC class I and class II molecules have similar structures -- 5-8.MHC class I binds shorter and more precisely defined peptides than MHC class II -- 5-9.MHC class I and class II bind peptides in different intracellular compartments -- 5-10.Peptides produced in the cytosol are transported to the endoplasmic reticulum for binding to MHC class I -- 5-11.MHC class I binds peptides in the context of a highly specific peptide-loading complex -- 5-12.All cells express MHC class I, whereas MHC class II is mainly expressed by professional antigen-presenting cells -- 5-13.Invariant chain prevents MHC class II from binding peptides in the endoplasmic reticulum -- 5-14.Cross-presentation enables extracellular antigens to be presented by MHC class I -- Summary -- The major histocompatibility complex -- 5-15.Human MHC diversity is the product of gene families and genetic polymorphisms -- 5-16.HLA class I and class II genes occupy separate regions of the HLA complex -- 5-17.Proteins involved in antigen processing and presentation are encoded by genes in the HLA class II region -- 5-18.Some MHC class I and class II genes are highly polymorphic -- 5-19.Selection by infectious disease is a likely major cause of HLA class I and class II diversity -- 5-20.Human populations all maintain a diversity of HLA class I and class II alleles -- Summary -- Summary to Chapter 5 -- Questions -- ch. 6 The Development of B Lymphocytes -- The development of B cells in the bone marrow -- 6-1.B-cell development in the bone marrow proceeds through several stages -- 6-2.B-cell development is stimulated by bone marrow stromal cells -- 6-3.Rearrangement of the immunoglobulin heavy-chain genes occurs in pro-B cells -- 6-4.The pre-B-cell receptor monitors the quality of immunoglobulin heavy chains -- 6-5.Rearrangement of the light-chain loci occurs in pre-B cells -- 6-6.B cells encounter two checkpoints during their development in the bone marrow -- 6-7.A program of protein expression underlies the stages of B-cell development -- 6-8.Many B-cell tumors have chromosomal translocations involving immunoglobulin genes -- 6-9.B cells expressing the cell-surface protein CD5 have a distinctive repertoire of receptors -- Summary -- Selection and further development of the B-cell repertoire -- 6-10.The immature B-cell population is purged of cells bearing self-reactive B-cell receptors -- 6-11.The antigen receptors of autoreactive immature B cells can be modified by receptor editing -- 6-12.Immature B cells that recognize monovalent self antigens are made nonresponsive -- 6-13.Maturation and survival of B cells occurs in lymphoid follicles -- 6-14.Encounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells -- 6-15.Different types of B-cell tumor reflect B cells at different stages of development -- Summary
Note continued: Summary to Chapter 6 -- Questions -- ch. 7 The Development of T Lymphocytes -- The development of T cells in the thymus -- 7-1.T cells develop in the thymus -- 7-2.Thymocytes commit to the T-cell lineage before rearranging their T-cell receptor genes -- 7-3.The two lineages of T cells arise from a common thymocyte progenitor -- 7-4.Gene rearrangement in double-negative thymocytes leads to assembly of either a [gamma delta] receptor or a pre-T-cell receptor -- 7-5.Rearrangement of the [alpha]-chain gene occurs only in pre-T cells -- 7-6.Stages in T-cell development are marked by changes in gene expression -- Summary -- Positive and negative selection of the T-cell repertoire -- 7-7.T cells that recognize self-MHC molecules undergo positive selection in the thymus -- 7-8.Positive selection is affected by peptides produced by a thymus-specific proteasome -- 7-9.Continuing a-chain gene rearrangement increases the chance of positive selection -- 7-10.Positive selection determines expression of either CD4 or CD8 -- 7-11.T cells specific for self antigens are removed in the thymus by negative selection -- 7-12.Tissue-specific proteins are expressed in the thymus and participate in negative selection -- 7-13.Regulatory CD4 T cells comprise a distinct lineage of CD4 T cells -- 7-14.T cells differentiate further after antigen recognition in secondary lymphoid tissue -- Summary -- Summary to Chapter 7 -- Questions -- ch. 8 T Cell-Mediated Immunity -- Activation of naive T cells by antigen -- 8-1.Dendritic cells carry antigens from sites of infection to secondary lymphoid tissues -- 8-2.Dendritic cells are adept and versatile at processing pathogen antigens -- 8-3.Naive T cells first encounter antigen presented by dendritic cells in secondary lymphoid tissues -- 8-4.Homing of naive T cells to secondary lymphoid tissues is determined by chemokines and cell-adhesion molecules -- 8-5.Activation of naive T cells requires signals from the antigen receptor and the co-stimulatory receptor -- 8-6.Signals from T-cell receptors, co-receptors, and co-stimulatory receptors activate naive T cells -- 8-7.Proliferation and differentiation of activated naive T cells are driven by the cytokine interleukin-2 -- 8-8.Antigen recognition in the absence of co-stimulation leads to a state of T-cell anergy -- 8-9.Activation of naive CD4 T cells gives rise to five types of effector CD4 T cell -- 8-10.The cytokine environment determines which differentiation pathway a naive T cell takes -- 8-11.Positive feedback in the cytokine environment can polarize the effector CD4 T-cell response -- 8-12.Naive CD8 T cells require stronger activation than that for naive CD4 T cells -- Summary -- The properties and functions of effector T cells -- 8-13.Cytotoxic CD8T cells and effector CD4 TH1, TH2, and TH17 cells work at sites of infection -- 8-14.Effector T-cell functions are mediated by cytokines and cytotoxins -- 8-15.Cytokines change the patterns of gene expression in the cells targeted by effector T cells -- 8-16.Cytotoxic CD8 T cells are selective and serial killers of target cells at sites of infection -- 8-17.Cytotoxic T cells kill their target cells by inducing apoptosis -- 8-18.Effector TH1 CD4 cells induce macrophage activation -- 8-19.Naive B cells and their helper TFH cells recognize different epitopes of the same antigen -- 8-20.Treg cells limit the activities of effector CD4 and CD8T cells -- Summary -- Summary to Chapter 8 -- Questions -- ch. 9 Immunity Mediated by B Cells and Antibodies -- Antibody production by B lymphocytes -- 9-1.B-cell activation requires cross-linking of the B-cell receptor -- 9-2.B-cell activation requires signals from the B-cell co-receptor -- 9-3.Effective B cell-mediated immunity depends on help from CD4 TFH cells -- 9-4.Follicular dendritic cells in the B-cell area store intact antigens and display them to B cells -- 9-5.Antigen-activated B cells move close to the T-cell area to find a TFH cell -- 9-6.The primary focus of clonal expansion in the medullary cords produces plasma cells secreting IgM -- 9-7.Somatic hypermutation and isotype switching occur in the specialized microenvironment of the primary follicle -- 9-8.Antigen-mediated selection of centrocytes drives affinity maturation of the B-cell response in the germinal center -- 9-9.Cytokines made by TFH cells guide B-cell switching of immunoglobulin isotype -- 9-10.TFH cells determine the differentiation of antigen-activated B cells into plasma cells or memory cells -- Summary -- Antibody effector functions -- 9-11.IgM, IgG, and monomeric IgA protect the internal tissues of the body -- 9-12.Dimeric IgA and pentameric IgM protect mucosal surfaces of the body -- 9-13.IgE provides a mechanism for rapid ejection of parasites and pathogens from the body -- 9-14.Before and after birth, mothers provide their children with protective antibodies -- 9-15.High-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells -- 9-16.High-affinity IgG and IgA antibodies neutralize microbial toxins and animal venoms -- 9-17.Binding of IgM to antigen on a pathogen's surface activates complement by the classical pathway -- 9-18.Two forms of C4 are fixed at different sites on pathogen surfaces -- 9-19.Complement activation by IgG requires the participation of two or more IgG molecules -- 9-20.Erythrocytes facilitate removal of immune complexes from the circulation -- 9-21.Fey receptors enable effector cells to bind IgG and be activated by IgG bound to pathogens -- 9-22.Several low-affinity Fc receptors are specific for IgG -- 9-23.An Fc receptor acts as an antigen receptor for NK cells -- 9-24.The Fc receptor for monomeric IgA 1 belongs to a different family than the Fc receptors for IgG and IgE -- Summary -- Summary to Chapter 9 -- Questions -- ch. 10 Preventing Infection at Mucosal Surfaces -- 10-1.The communication functions of mucosal surfaces render them vulnerable to infection -- 10-2.Mucins are gigantic glycoproteins that endow the mucus with properties to protect epithelial surfaces -- 10-3.Commensal microorganisms assist the gut in digesting food and maintaining health -- 10-4.The gastrointestinal tract is invested with distinctive secondary lymphoid tissues -- 10-5.Inflammation of mucosal tissues is associated with causation not cure of disease -- 10-6.Intestinal epithelial cells contribute to innate immune responses in the gut -- 10-7.Intestinal macrophages eliminate pathogens without creating a state of inflammation -- 10-8.M cells transport microbes and antigens from the gut lumen to gut-associated lymphoid tissue -- 10-9.Gut dendritic cells respond differently to food antigens, commensal microorganisms, and pathogens -- 10-10.Activation of B cells and T cells in one mucosal tissue commits them to defending all mucosal tissues -- 10-11.A variety of effector lymphocytes guard healthy mucosal tissue in the absence of infection -- 10-12.B cells activated in mucosal tissues give rise to plasma cells secreting IgM and IgA at mucosal surfaces -- 10-13.Secretory IgM and IgA protect mucosal surfaces from microbial invasion -- 10-14.Two subclasses of IgA have complementary properties for controlling microbial populations -- 10-15.People lacking IgA are able to survive, reproduce, and be generally healthy -- Summary to Chapter 10 -- Questions -- ch. 11 Immunological Memory and Vaccination -- Immunological memory and the secondary immune response -- 11-1.Immunological memory is essential for the survival of human populations -- 11-2.Antibodies made in a primary response persist in the circulation to prevent reinfection -- 11-3.Memory B cells, naive B cells, and plasma cells are distinguished by the expression of their B-cell receptors -- 11-4.Immune complex-mediated inhibition of naive B cells is used to prevent hemolytic anemia of the newborn -- 11-5.Long-lived plasma cells are the major mediators of B-cell memory -- 11-6.In responses to influenza virus, immunological memory is gradually lost with successive infections -- 11-7.Antigen-mediated activation of naive T cells gives rise to effector and memory T cells -- 11-8.Two subpopulations of circulating memory cells patrol different tissues of the body -- 11-9.Primary infections of a non-lymphoid tissue produce resident memory T cells that live within the tissue -- 11-10.Resident memory T cells are the most numerous type of memory T cell -- Summary -- Vaccination to prevent infectious disease -- 11-11.Protection against smallpox is achieved by immunization with the less dangerous vaccinia virus -- 11-12.Smallpox is the only infectious disease of humans that has been eradicated worldwide by vaccination -- 11-13.Most viral vaccines are made from killed or inactivated viruses -- 11-14.Both inactivated and live-attenuated vaccines protect against poliovirus -- 11-15.Vaccination can inadvertently cause disease -- 11-16.Subunit vaccines are made from the most antigenic components of a pathogen -- 11-17.Invention and application of rotavirus vaccines took decades of research and development -- 11-18.Bacterial vaccines are made from whole bacteria, secreted toxins, or capsular polysaccharides -- 11-19.Conjugate vaccines enable high-affinity antibodies to be made against carbohydrate antigens -- 11-20. Adjuvants are added to vaccines to activate and enhance the immune response to a pathogen -- 11-21.Genome sequences of human pathogens have opened up new avenues for making vaccines -- 11-22.The rapidly evolving influenza virus requires continual vaccine development -- 11-23.The need for a vaccine and the demands placed upon it change with the prevalence of disease -- 11-24.Vaccines have yet to be made against pathogens that establish chronic infections -- 11-25.Vaccine development faces greater public scrutiny than does drug development -- Summary -- Summary to Chapter 11 -- Questions -- ch. 12 Coevolution of Innate and Adaptive Immunity
Note continued: Regulation of NK-cell function by MHC class I and related molecules -- 12-1.NK cells express a range of activating and inhibitory receptors -- 12-2.Fc receptor expression enables NK cells to participate in the adaptive immune response -- 12-3.A variety of NK-cell receptors recognize MHC class I and structurally related surface glycoproteins -- 12-4.Immunoglobulin-like NK-cell receptors recognize polymorphic epitopes of HLA-A, -B, and -C -- 12-5.NK cells are educated to detect pathological changes in MHC class I expression -- 12-6.Different genomic complexes encode lectin-like and immunoglobulin-like receptors for HLA class I -- 12-7.There are two distinctive forms of human KIR haplotypes -- 12-8.Cytomegalovirus infection induces proliferation of NK cells expressing the activating HLA-E receptor -- 12-9.Interactions of uterine NK cells with fetal MHC class I molecules affect reproductive success -- Summary -- Maintenance of tissue integrity by [gamma delta] T cells -- 12-10.[gamma delta] T cells are not subject to the same constraints as [alpha beta]T cells -- 12-11.[gamma delta] T cells in blood and tissues express different [gamma delta] receptors -- 12-12.V[sub gamma]9:V[sub delta]2 T cells respond to phosphoantigens bound by butyrophilins -- 12-13.V[sub gamma]4:V[sub delta]5 T cells detect both virus-infected cells and tumor cells -- 12-14.[gamma delta] T-cell receptors combine properties of the receptors of innate and adaptive immunity -- 12-15.V[sub gamma]:V[sub delta]1 T-cell receptors recognize lipid antigens presented by CD1d -- Summary -- Restriction of ab T cells by nonpolymorphic MHC class I -- like molecules -- 12-16.CD1-restricted [alpha beta] T cells recognize lipid antigens of mycobacteria -- 12-17.NKT cells are innate lymphocytes with [alpha beta] T-cell receptors that recognize lipid antigens -- 12-18.Mucosa-associated invariant T cells detect bacteria and fungi that make riboflavin -- Summary -- Summary to Chapter 12 -- Questions -- ch. 13 Failures of the Body's Defenses -- Evasion and subversion of the immune system by pathogens -- 13-1.Genetic variation within some species of pathogens prevents effective long-term immunity -- 13-2.Mutation and recombination allow influenza virus to escape from immunity -- 13-3.Trypanosomes use gene conversion to change their surface antigens -- 13-4.Herpesviruses persist in human hosts by hiding from the immune response -- 13-5.Human herpesviruses cause a variety of diseases -- 13-6.Some bacteria and parasites subvert the human immune response -- 13-7.Bacterial superantigens stimulate a massive 1 but ineffective CD4 T-cell response -- 13-8.Subversion of IgA by bacterial IgA-binding proteins -- Summary -- Inherited immunodeficiency diseases -- 13-9.Rare primary immunodeficiency diseases reveal how the human immune system works -- 13-10.Inherited immunodeficiency diseases are caused by dominant, recessive, or X-linked gene defects -- 13-11.Recessive and dominant mutations in the IFN-y receptor cause immunodeficiency of differing severity -- 13-12.Antibody deficiency leads to poor clearing of extracellular bacteria -- 13-13.Diminished production of antibodies can arise from inherited defects in T-cell help -- 13-14.Complement defects impair antibody-mediated immunity and cause immune-complex disease -- 13-15.Defects in phagocytes cause enhanced susceptibility to bacterial infection -- 13-16.Defects in T-cell function underlie severe combined immunodeficiencies -- 13-17.Some inherited immunodeficiencies cause susceptibility to particular pathogens -- Summary -- Acquired immune deficiency syndrome -- 13-18.HIV is a retrovirus that causes a slowly progressing chronic disease -- 13-19.Human immune systems are better adapted to HIV-2 than to HIV-1 -- 13-20.HIV infects CD4 T cells, macrophages, and dendritic cells -- 13-21.In the 20th century most HIV infections progressed to AIDS -- 13-22.Genetic deficiency of the CCR5 co-receptor for HIV confers resistance to infection -- 13-23.HLA and KIR polymorphisms influence progression to AIDS -- 13-24.HIV resists the immune response and gains resistance to antiviral drugs through rapid mutation -- 13-25.Clinical latency is a period of active infection and renewal of CD4 T cells -- 13-26.HIV infection leads to immunodeficiency and death from opportunistic infections -- 13-27.A minority of HIV-infected individuals make antibodies that neutralize many strains of HIV -- Summary -- Summary to Chapter 13 -- Questions -- ch. 14 Allergy and the Immune Response to Parasites -- 14-1.Different effector mechanisms underlie the four types of hypersensitivity reaction -- Shared mechanisms of immunity and allergy -- 14-2.Th2 immune responses defend the body against infestation with multicellular parasites -- 14-3.Allergy prevails in the industrialized countries where parasite infections have been eradicated -- 14-4.Basophils initiate the Th2 response -- 14-5.IgE antibodies emerge at early and late times in the primary immune response -- 14-6.IgE differs in structure and function from other immunoglobulin isotypes -- 14-7.Together, IgE and FceRI arm each mast cell with a high diversity of antigen-specific receptors -- 14-8.FceRII is expressed by B cells and regulates the production of IgE -- 14-9.Allergic disease can be treated with an IgE-specific monoclonal antibody -- 14-10.Mast cells defend and maintain the tissues in which they reside -- 14-11.Mast cells in tissues orchestrate IgE-mediated reactions through the release of inflammatory mediators -- 14-12.Eosinophils are specialized granulocytes that release toxic mediators in IgE-mediated immune responses -- Summary -- IgE-mediated allergic disease -- 14-13.Allergens are protein antigens that can resemble parasite antigens -- 14-14.Predisposition to allergic disease is influenced by genetic and environmental factors -- 14-15.IgE-mediated allergic reactions consist of an immediate response followed by a late-phase response -- 14-16.The effects of IgE-mediated allergic reactions vary with the site of mast-cell activation -- 14-17.Systemic anaphylaxis is caused by allergens in the blood -- 14-18.Rhinitis and asthma are caused by inhaled allergens -- 14-19.Urticaria and angioedema are allergic reactions in the skin -- 14-20.Atopic dermatitis is a chronic disease affecting the skin that has multiple risk factors -- 14-21.Food allergies cause systemic effects as well as gut reactions -- 14-22.Allergic reactions are prevented and treated by three complementary approaches -- Summary -- Summary to Chapter 14 -- Questions -- ch. 15 Transplantation of Tissues and Organs -- Allogeneic transplantation can trigger hypersensitivity reactions -- 15-1.Blood is the most commonly transplanted tissue -- 15-2.Incompatibility of blood group antigens causes type II hypersensitivity reactions -- 15-3.Hyperacute rejection of transplanted organs is a type II hypersensitivity reaction -- 15-4.Anti-HLA antibodies arise from pregnancy, blood transfusion, and transplantation -- 15-5.Acute transplant rejection and graft-versus-host disease are type IV hypersensitivity reactions -- Summary -- Transplantation of solid organs -- 15-6.Organ transplantation involves procedures that produce inflammation in the donated organ and the transplant recipient -- 15-7.HLA differences between transplant donor and recipient activate numerous alloreactive T cells -- 15-8.Acute rejection is a type IV hypersensitivity caused by T cells responding to HLA differences between donor and recipient -- 15-9.Chronic rejection of transplanted organs is equivalent to a type III hypersensitivity reaction -- 15-10.Matching donor and recipient HLA class I and class II allotypes improves the outcome of kidney transplantation -- 15-11.Immunosuppressive drugs enable allogeneic kidney transplantation to be a routine therapy -- 15-12.Immunosuppression is given before and after kidney transplantation -- 15-13.T-cell activation by alloantigens can be specifically prevented by immunosuppressive drugs -- 15-14.Blocking cytokine signaling prevents the activation of alloreactive T cells -- 15-15.Cytotoxic drugs target the replication and proliferation of activated alloreactive T cells -- 15-16.Patients needing a transplant outnumber the available organs -- 15-17.The need for HLA matching and immunosuppressive therapy varies with the organ transplanted -- Summary -- Hematopoietic cell transplantation -- 15-18.Hematopoietic cell transplantation is a treatment for genetic diseases of blood cells -- 15-19.Allogeneic hematopoietic cell transplantation is the preferred treatment for many cancers -- 15-20.After hematopoietic cell transplantation, the patient is attacked by alloreactive T cells in the graft -- 15-21.HLA matching of donor and recipient is most important for hematopoietic cell transplantation -- 15-22.Minor histocompatibility antigens activate alloreactive T cells in recipients of HLA-identical transplants -- 15-23.Some GVHD helps engraftment and prevents relapse of malignant disease -- 15-24.NK cells mediate graft-versus-leukemia effects -- 15-25.Hematopoietic cell transplantation can induce tolerance of a solid organ transplant -- Summary -- Summary to Chapter 15 -- Questions -- ch. 16 Disruption of Healthy Tissue by the Adaptive Immune Response -- 16-1.Every autoimmune disease resembles a type II, III, or IV hypersensitivity reaction -- 16-2.Autoimmune diseases arise when tolerance to self antigens is lost -- 16-3.Most autoimmune responses and diseases are initiated by autoreactive Th17 CD4T cells -- 16-4.HLA is the dominant genetic factor affecting susceptibility to autoimmune disease -- 16-5.Autoimmune disease is more prevalent in women than in men -- 16-6.HLA associations reflect the importance of T-cell tolerance in preventing autoimmunity -- 16-7.Binding of antibody to a cell-surface receptor can cause an autoimmune disease -- 16-8.Tertiary lymphoid tissue forms in tissues inflamed by autoimmune disease
Note continued: 16-9.The antibody response to an autoantigen can broaden and strengthen by epitope spreading -- 16-10.Intermolecular epitope spreading occurs in systemic autoimmune disease -- 16-11.Intravenous immunoglobulin is a therapy for autoimmune diseases -- 16-12.Monoclonal antibodies that target TNF-[alpha] and B cells are used to treat rheumatoid arthritis -- 16-13.Rheumatoid arthritis is associated with genetic and environmental factors -- 16-14.An autoimmune disease caused by physical trauma -- 16-15.Type 1 diabetes is caused by selective destruction of insulin-producing cells of the pancreas -- 16-16.Combinations of HLA class II allotypes confer susceptibility and resistance to type 1 diabetes -- 16-17.Celiac disease is a hypersensitivity to food that has much in common with autoimmune disease -- 16-18.Celiac disease is caused by the selective destruction of intestinal epithelial cells -- 16-19.Senescence of the thymus and the T-cell population contributes to autoimmunity -- Summary to Chapter 16 -- Questions -- ch. 17 Cancer, Immunity, and Immunotherapy -- The evolution of cancer from healthy human cells -- 17-1.Cancer results from mutations that cause uncontrolled cell growth -- 17-2.Cancer arises from a cell that has accumulated multiple mutations -- 17-3.Exposure to chemicals, radiation, and viruses facilitates progression to cancer -- 17-4.Common features of cancer cells distinguish them from normal cells -- Human immune responses to cancer -- 17-5.Immune responses to cancer have similarities to those made against virus-infected cells -- 17-6.Mutations acquired by somatic cells during oncogenesis give rise to tumor-specific antigens -- 17-7.Cancer/testis antigens are a prominent class of tumor-associated antigen -- 17-8.Control of cancer by the immune system does not require elimination of all the tumor cells -- 17-9.Successful tumors are ones that evade and manipulate the immune response -- 17-10.Vaccination against human papillomavirus antigens prevents the occurrence of genital cancers -- Controlling cancer with immunotherapy -- 17-11.Monoclonal antibodies are valuable tools for the diagnosis of cancer -- 17-12.Monoclonal antibodies against cell-surface antigens are increasingly used in cancer immunotherapy -- 17-13.Monoclonal antibodies specific for inhibitory regulators of T-cell responses are effective therapies for cancer -- 17-14.Adoptive cell transfer improves the natural T-cell response to a tumor -- 17-15.T-cell responses to tumor cells can be improved using chimeric antigen receptors -- 17-16.T-cell responses to tumors can be improved by adoptive transfer of antigen-activated dendritic cells -- Summary to Chapter 17 -- Questions
Summary "A clear, concise, and contemporary presentation of immunological concepts. This text emphasizes the human immune system and presents concepts with a balanced level of detail to describe how the immune system works. Written for undergraduate, medical, veterinary, dental, and pharmacy students, it makes generous use of medical examples to illustrate points. This classroom-proven textbook offers clear writing, full-color illustrations, and section and chapter summaries that make the content accessible and easily understandable to students."-- Provided by publisher
Bibliography Includes bibliographical references and index
Subject Immune system
Immune System Phenomena
Immune System
Immune system
Genre/Form Textbooks.
LC no. 2020047308
ISBN 9780393533354