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005 20211227074408.0
008 140702t20152015nyua b 001 0 eng
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050 00 $aQR181$b.P335 2015
060 00 $a2014 N-020
060 10 $aQW 504
060 4 $aQW 504$bP229i 2015
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084 $aMED044000$aSCI007000$aSCI008000$2bisacsh
084 $aQ3$qUkBrU-I$2cmedlit
100 1 $aParham, Peter,$d1950-$eauthor.
245 14 $aThe immune system /$cPeter Parham.
250 $aFourth edition.
264 1 $aNew York, NY :$bGarland Science, Taylor & Francis Group,$c[2015]
264 4 $c©2015
300 $a1 volume (various pagings) :$billustrations (chiefly color) ;$c28 cm
336 $atext$btxt$2rdacontent
337 $aunmediated$bn$2rdamedia
338 $avolume$bnc$2rdacarrier
500 $a"The Immune system is adapted from Janeway's Immunobiology, also published by Garland Science."
520 $a"The Immune System, Fourth Edition, emphasizes the human immune system and synthesizes immunological concepts into a coherent, up-to-date, and reader-friendly account of how the immune system works. Written for undergraduate, medical, veterinary, dental, and pharmacy students, it makes generous use of medical examples to illustrate points. The Fourth Edition has been extensively revised and updated. Innate immunity has undergone major revision to reflect this expanding and fast-moving field, and is now divided between two chapters: Chapter 2 "Innate Immunity: The Immediate Response to Infection," which deals with complement and other soluble molecules of innate immunity such as antimicrobial peptides, and Chapter 3 "Innate Immunity: The Induced Response to Infection," which deals mainly with the cellular response. Chapters 4-9 have been updated and material has been consolidated to eliminate repetition. Mucosal immunology has exploded as a field since the Third Edition was published, thus its coverage in chapter 10, now devoted to the topic, has been significantly expanded and updated. Also, more emphasis is placed on commensal microorganisms, particularly of the gut, and their interactions with the immune system. Immunological memory and the secondary immune response is now the first part of Chapter 11. The second part of this chapter, entitled "Vaccination to Prevent Infectious Disease," will include new and more modern material. "Bridging Innate and Adaptive Immunity" will also have its own chapter. The remaining clinical chapters will be revised and updated with new immunotherapies, but their content and organization will remain largely the same. The Fourth Edition will be accompanied by an updated and greatly expanded question bank, as well as PowerPoints and JPEGs of all the figures in the text."--$cProvided by publisher.
504 $aIncludes bibliographical references and index.
505 0 $aElements in the immune system and their roles in defense -- Innate immunity : the immediate response to infection -- Innate immunity : the induced response to infection -- Antibody structure and the generation of B-cell diversity -- Antigen recognition by T lymphocytes -- The development of B lymphocytes -- The development of T lymphocytes -- T cell-mediated immunity -- Immunity mediated by B cells and antibodies -- Preventing infection at mucosal surfaces -- Immunological memory and vaccination -- Coevolution of innate and adaptive immunity -- Failures of the body's defenses -- IgE-mediated immunity and allergy -- Transplantation of tissues and organs -- Disruption of healthy tissue by the adaptive immune response -- Cancer and its interactions with the immune system.
650 0 $aImmune system.
650 0 $aImmunopathology.
650 7 $aMEDICAL$xImmunology.$2bisacsh
650 7 $aSCIENCE$xLife Sciences$xBiochemistry.$2bisacsh
650 7 $aSCIENCE$xLife Sciences$xBiology$xGeneral.$2bisacsh
650 7 $aImmune system.$2fast$0(OCoLC)fst00967877
650 7 $aImmunopathology.$2fast$0(OCoLC)fst00968028
650 12 $aImmune System
650 22 $aImmunity
650 22 $aImmune System Phenomena
700 1 $aJaneway, Charles.$tImmunobiology.$iBased on.
776 08 $iOnline version:$aParham, Peter, 1950-$tImmune system.$bFourth edition$w(OCoLC)1195553302
856 42 $uhttps://online.vitalsource.com/#/books/9781317511571/cfi/0!/4/4@0.00:0.00
856 42 $3Cover image$uhttp://images.tandf.co.uk/common/jackets/websmall/978081534/9780815344667.jpg
880 00 $6505-00/(S$aContents note continued:$g11-15.$tSmallpox is the only infectious disease of humans that has been eradicated worldwide by vaccination --$g11-16.$tMost viral vaccines are made from killed or inactivated viruses --$g11-17.$tBoth inactivated and live-attenuated vaccines protect against poliovirus --$g11-18.$tVaccination can inadvertently cause disease --$g11-19.$tSubunit vaccines are made from the most antigenic components of a pathogen --$g11-20.$tInvention of rotavirus vaccines took at least 30 years of research and development --$g11-21.$tBacterial vaccines are made from whole bacteria, secreted toxins, or capsular polysaccharides --$g11-22.$tConjugate vaccines enable high-affinity antibodies to be made against carbohydrate antigens --$g11-23.$tAdjuvants are added to vaccines to activate and enhance the response to antigen --$g11-24.$tGenome sequences of human pathogens have opened up new avenues for making vaccines --$g11-25.$tever-changing influenza virus requires a new vaccine every year --$g11-26.$tneed for a vaccine and the demands placed upon it change with the prevalence of disease --$g11-27.$tVaccines have yet to be made against pathogens that establish chronic infections --$g11-28.$tVaccine development faces greater public scrutiny than drug development --$tSummary --$tSummary to Chapter 11 --$tQuestions --$gch. 12$tCoevolution of Innate and Adaptive Immunity --$tRegulation of NK-cell function by MHC class I and related molecules --$g12-1.$tNK cells express a range of activating and inhibitory receptors --$g12-2.$tstrongest receptor that activates NK cells is an Fc receptor --$g12-3.$tMany NK-cell receptors recognize MHC class I and related molecules --$g12-4.$tImmunoglobulin-like NK-cell receptors recognize polymorphic epitopes of HLA-A, HLA-B, and HLA-C --$g12-5.$tNK cells are educated to detect pathological change in MHC class I expression --$g12-6.$tDifferent genomic complexes encode lectin-like and immunoglobulin-like NK-cell receptors --$g12-7.$tHuman KIR haplotypes uniquely come in two distinctive forms --$g12-8.$tCytomegalovirus infection induces proliferation of NK cells expressing the activating HLA-E receptor --$g12-9.$tInteractions of uterine NK cells with fetal MHC class I molecules affect reproductive success --$tSummary --$tMaintenance of tissue integrity by γ:δ T cells --$g12-10.$tγ:δ T cells are not governed by the same rules as α:β T cells --$g12-11.$tγ:δ T cells in blood and tissues express different γ:δ receptors --$g12-12.$tVγ9:Vγ2 T cells recognize phosphoantigens presented on cell surfaces --$g12-13.$tVγ4:Vγ5 T cells detect both virus-infected cells and tumor cells --$g12-14.$tVγ:Vγ1 T-cell receptors recognize lipid --$tAntigens presented by CD1d --$tSummary --$tRestriction of α:β T cells by non-polymorphic MHC class l-like molecules --$g12-15.$tCD 1-restricted α:β T cells recognize lipid antigens of mycobacterial pathogens --$g12-16.$tNKT cells are innate lymphocytes that detect lipid antigens by using α:β T-cell receptors --$g12-17.$tMucosa-associated invariant T cells detect bacteria and fungi that make riboflavin --$tSummary --$tSummary to Chapter 12 --$tQuestions --$gch. 13$tFailures of the Body's Defenses --$tEvasion and subversion of the immune system by pathogens --$g13-1.$tGenetic variation within some species of pathogens prevents effective long-term immunity --$g13-2.$tMutation and recombination allow influenza virus to escape from immunity --$g13-3.$tTrypanosomes use gene conversion to change their surface antigens --$g13-4.$tHerpesviruses persist in human hosts by hiding from the immune response --$g13-5.$tSome pathogens sabotage or subvert immune defense mechanisms --$g13-6.$tBacterial superantigens stimulate a massive but ineffective CD4 T-cell response --$g13-7.$tSubversion of IgA action by bacterial IgA-binding proteins --$tSummary --$tInherited immunodeficiency diseases --$g13-8.$tRare primary immunodeficiency diseases reveal how the human immune system works --$g13-9.$tInherited immunodeficiency diseases are caused by dominant, recessive, or X-linked gene defects --$g13-10.$tRecessive and dominant mutations in the IFN-γ receptor cause diseases of differing severity --$g13-11.$tAntibody deficiency leads to poor clearing of extracellular bacteria --$g13-12.$tDiminished production of antibodies also results from inherited defects in T-cell help --$g13-13.$tComplement defects impair antibody-mediated immunity and cause immune-complex disease --$g13-14.$tDefects in phagocytes result in enhanced susceptibility to bacterial infection --$g13-15.$tDefects in T-cell function result in severe combined immune deficiencies --$g13-16.$tSome inherited immunodeficiencies lead to specific disease susceptibilities --$tSummary --$tAcquired immune deficiency syndrome --$g13-17.$tHIV is a retrovirus that causes a slowly progressing chronic disease --$g13-18.$tHIV infects CD4 T cells, macrophages, and dendritic cells --$g13-19.$tIn the twentieth century, most HIV-infected people progressed in time to get AIDS --$g13-20.$tGenetic deficiency of the CCR5 co-receptor --$tFor HIV confers resistance to infection --$g13-21.$tHLA and KIR polymorphisms influence the progression to AIDS --$g13-22.$tHIV escapes the immune response and develops resistance to antiviral drugs by rapid mutation --$g13-23.$tClinical latency is a period of active infection and renewal of CD4 T cells --$g13-24.$tHIV infection leads to immunodeficiency and death from opportunistic infections --$g13-25.$tminority of HIV-infected individuals make antibodies that neutralize many strains of HIV --$tSummary --$tSummary to Chapter 13 --$tQuestions --$gch. 14$tIgE-Mediated Immunity and Allergy --$g14-1.$tDifferent effector mechanisms cause four distinctive types of hypersensitivity reaction --$tShared mechanisms of immunity and allergy --$g14-2.$tIgE-mediated immune responses defend the body against multicellular parasites --$g14-3.$tIgE antibodies emerge at early and late times in the primary immune response --$g14-4.$tAllergy is prevalent in countries where parasite infections have been eliminated --$g14-5.$tIgE has distinctive properties that contrast with those of IgG --$g14-6.$tIgE and FcεRI supply each mast cell with a diversity of antigen-specific receptors --$g14-7.$tFcεRII is a low-affinity receptor for IgE Fc regions that regulates the production of IgE by B cells --$g14-8.$tTreatment of allergic disease with an IgE-specific monoclonal antibody --$g14-9.$tMast cells defend and maintain the tissues in which they reside --$g14-10.$tTissue mast cells orchestrate IgE-mediated reactions through the release of inflammatory mediators --$g14-11.$tEosinophils are specialized granulocytes that release toxic mediators in IgE-mediated responses --$g14-12.$tBasophils are rare granulocytes that initiate TH2 responses and the production of IgE --$tSummary --$tIgE-mediated allergic disease --$g14-13.$tAllergens are protein antigens, some of which resemble parasite antigens --$g14-14.$tPredisposition to allergic disease is influenced by genetic and environmental factors --$g14-15.$tIgE-mediated allergic reactions consist of an immediate response followed by a late-phase response --$g14-16.$teffects of IgE-mediated allergic reactions vary with the site of mast-cell activation --$g14-17.$tSystemic anaphylaxis is caused by allergens in the blood --$g14-18.$tRhinitis and asthma are caused by inhaled allergens --$g14-19.$tUrticaria, angioedema, and eczema are allergic reactions in the skin --$g14-20.$tFood allergies cause systemic effects as well as gut reactions --$g14-21.$tAllergic reactions are prevented and treated by three complementary approaches --$tSummary --$tSummary to Chapter 14 --$tQuestions --$gch. 15$tTransplantation of Tissues and Organs --$tAllogeneic transplantation can trigger hypersensitivity reactions --$g15-1.$tBlood is the most common transplanted tissue --$g15-2.$tBefore blood transfusion, donors and recipients are matched for ABO and the Rhesus D antigens --$g15-3.$tIncompatibility of blood group antigens causes type II hypersensitivity reactions --$g15-4.$tHyperacute rejection of transplanted organs is a type II hypersensitivity reaction --$g15-5.$tAnti-HLA antibodies can arise from pregnancy, blood transfusion, or previous transplants --$g15-6.$tTransplant rejection and graft-versus-host disease are type IV hypersensitivity reactions --$tSummary --$tTransplantation of solid organs --$g15-7.$tOrgan transplantation involves procedures that inflame the donated organ and the transplant recipient --$g15-8.$tAcute rejection is a type IV hypersensitivity caused by effector T cells responding to HLA differences between donor and recipient --$g15-9.$tHLA differences between transplant donor and recipient activate numerous alloreactive T cells --$g15-10.$tChronic rejection of organ transplants is caused by a type III hypersensitivity reaction --$g15-11.$tMatching donor and recipient HLA class I and II allotypes improves the success of transplantation --$g15-12.$tImmunosuppressive drugs make allogeneic transplantation possible as routine therapy --$g15-13.$tSome treatments induce immune-suppression before transplantation --$g15-14.$tT-cell activation can be targeted by immunosuppressive drugs --$g15-15.$tAlloreactive T-cell co-stimulation can be blocked with a soluble form of CTLA4 --$g15-16.$tBlocking cytokine signaling can prevent alloreactive T-cell activation --$g15-17.$tCytotoxic drugs target the replication and proliferation of alloantigen-activated T cells --$g15-18.$tPatients needing a transplant outnumber the available organs --$g15-19.$tneed for HLA matching and immunosuppressive therapy varies with the organ transplanted --
880 00 $6505-00/(S$aContents note continued:$g6-12.$tantigen receptors of autoreactive immature B cells can be modified by receptor editing --$g6-13.$tImmature B cells specific for monovalent self antigens are made nonresponsive to antigen --$g6-14.$tMaturation and survival of B cells requires access to lymphoid follicles --$g6-15.$tEncounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells --$g6-16.$tDifferent types of B-cell tumor reflect B cells at different stages of development --$tSummary --$tSummary to Chapter 6 --$tQuestions --$gch. 7$tDevelopment of T Lymphocytes --$g7-1.$tT cells develop in the thymus --$g7-2.$tThymocytes commit to the T-cell lineage before rearranging their T-cell receptor genes --$g7-3.$ttwo lineages of T cells arise from a common thymocyte progenitor --$g7-4.$tGene rearrangement in double-negative thymocytes leads to assembly of either a y:8 receptor or a pre-T-cell receptor --$g7-5.$tThymocytes can make four attempts to rearrange a β-chain gene --$g7-6.$tRearrangement of the a-chain gene occurs only in pre-T cells --$g7-7.$tStages in T-cell development are marked by changes in gene expression --$tSummary --$tPositive and negative selection of the T-cell repertoire --$g7-8.$tT cells that recognize self-MHC molecules are positively selected in the thymus --$g7-9.$tContinuing α-chain gene rearrangement increases the chance for positive selection --$g7-10.$tPositive selection determines expression of either the CD4 or the CD8 co-receptor --$g7-11.$tT cells specific for self antigens are removed in the thymus by negative selection --$g7-12.$tTissue-specific proteins are expressed in the thymus and participate in negative selection --$g7-13.$tRegulatory CD4 T cells comprise a distinct lineage of CD4T cells --$g7-14.$tT cells undergo further differentiation in secondary lymphoid tissues after encounter with antigen --$tSummary --$tSummary to Chapter 7 --$tQuestions --$gch. 8$tT Cell-Mediated Immunity --$tActivation of naive T cells by antigen --$g8-1.$tDendritic cells carry antigens from sites of infection to secondary lymphoid tissues --$g8-2.$tDendritic cells are adept and versatile at processing pathogen antigens --$g8-3.$tNaive T cells first encounter antigen presented by dendritic cells in secondary lymphoid tissues --$g8-4.$tHoming of naive T cells to secondary lymphoid tissues is determined by chemokines and cell-adhesion molecules --$g8-5.$tActivation of naive T cells requires signals from the antigen receptor and a co-stimulatory receptor --$g8-6.$tSignals from T-cell receptors, co-receptors, and co-stimulatory receptors activate naive T cells --$g8-7.$tProliferation and differentiation of activated naive T cells are driven by the cytokine interleukin-2 --$g8-8.$tAntigen recognition in the absence of co-stimulation leads to a state of T-cell anergy --$g8-9.$tActivation of naive CD4 T cells gives rise to effector CD4 T cells with distinctive helper functions --$g8-10.$tcytokine environment determines which differentiation pathway a naive T cell takes --$g8-11.$tPositive feedback in the cytokine environment can polarize the effector CD4 T-cell response --$g8-12.$tNaive CD8 T cells require stronger activation than naive CD4 T cells --$tSummary --$tproperties and functions of effector T cells --$g8-13.$tCytotoxic CD8 T cells and effector CD4 TH1, TH2, and TH17 work at sites of infection --$g8-14.$tEffector T-cell functions are mediated by cytokines and cytotoxins --$g8-15.$tCytokines change the patterns of gene expression in the cells targeted by effector T cells --$g8-16.$tCytotoxic CD8 T cells are selective and serial killers of target cells at sites of infection --$g8-17.$tCytotoxic T cells kill their target cells by inducing apoptosis --$g8-18.$tEffector TH1 CD4 cells induce macrophage activation --$g8-19.$tTFH cells, and the naive B cells that they help, recognize different epitopes of the same antigen --$g8-20.$tRegulatory CD4 T cells limit the activities of effector CD4 and CD8T cells --$tSummary --$tSummary to Chapter 8 --$tQuestions --$gch. 9$tImmunity Mediated by B Cells and Antibodies --$tAntibody production by B lymphocytes --$g9-1.$tB-cell activation requires cross-linking of surface immunoglobulin --$g9-2.$tB-cell activation requires signals from the B-cell co-receptor --$g9-3.$tEffective B cell-mediated immunity depends on help from CD4 T cells --$g9-4.$tFollicular dendritic cells in the B-cell area store and display intact antigens to B cells --$g9-5.$tAntigen-activated B cells move close to the T-cell area to find a helper TFH cell --$g9-6.$tprimary focus of clonal expansion in the medullary cords produces plasma cells secreting IgM --$g9-7.$tActivated B cells undergo somatic hypermutation and isotype switching in the specialized microenvironment of the primary follicle --$g9-8.$tAntigen-mediated selection of centrocytes drives affinity maturation of the B-cell response in the germinal center --$g9-9.$tcytokines made by helper T cells determine how B cells switch their immunoglobulin isotype --$g9-10.$tCytokines made by helper T cells determine the differentiation of antigen-activated B cells into plasma cells or memory cells --$tSummary --$tAntibody effector functions --$g9-11.$tIgM, IgG, and monomeric IgA protect the internal tissues of the body --$g9-12.$tDimeric IgA protects the mucosal surfaces of the body --$g9-13.$tIgE provides a mechanism for the rapid ejection of parasites and other pathogens from the body --$g9-14.$tMothers provide protective antibodies to their young, both before and after birth --$g9-15.$tHigh-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells --$g9-16.$tHigh-affinity IgG and IgA antibodies are used to neutralize microbial toxins and animal venoms --$g9-17.$tBinding of IgM to antigen on a pathogen's surface activates complement by the classical pathway --$g9-18.$tTwo forms of C4 tend to be fixed at different sites on pathogen surfaces --$g9-19.$tComplement activation by IgG requires the participation of two or more IgG molecules --$g9-20.$tErythrocytes facilitate the removal of immune complexes from the circulation --$g9-21.$tFey receptors enable effector cells to bind and be activated by IgG bound to pathogens --$g9-22.$tvariety of low-affinity Fc receptors are IgG-specific --$g9-23.$tFc receptor acts as an antigen receptor for NK cells --$g9-24.$tFc receptor for monomeric IgA belongs to a different family than the Fc receptors for IgG and IgE --$tSummary --$tSummary to Chapter 9 --$tQuestions --$gch. 10$tPreventing Infection at Mucosal Surfaces --$g10-1.$tcommunication functions of mucosal surfaces render them vulnerable to infection --$g10-2.$tMucins are gigantic glycoproteins that endow the mucus with the properties to protect epithelial surfaces --$g10-3.$tCommensal microorganisms assist the gut in digesting food and maintaining health --$g10-4.$tgastrointestinal tract is invested with distinctive secondary lymphoid tissues --$g10-5.$tInflammation of mucosal tissues is associated with causation not cure of disease --$g10-6.$tIntestinal epithelial cells contribute to innate immune responses in the gut --$g10-7.$tIntestinal macrophages eliminate pathogens without creating a state of inflammation --$g10-8.$tM cells constantly transport microbes and antigens from the gut lumen to gut-associated lymphoid tissue --$g10-9.$tGut dendritic cells respond differently to food, commensal microorganisms, and pathogens --$g10-10.$tActivation of B cells and T cells in one mucosal tissue commits them to defending all mucosal tissues --$g10-11.$tvariety of effector lymphocytes guard healthy mucosal tissue in the absence of infection --$g10-12.$tB cells activated in mucosal tissues give rise to plasma cells secreting IgM and IgA at mucosal surfaces --$g10-13.$tSecretory IgM and IgA protect mucosal surfaces from microbial invasion --$g10-14.$tTwo subclasses of IgA have complementary properties for controlling microbial populations --$g10-15.$tPeople lacking IgA are able to survive, reproduce, and generally remain healthy --$g10-16.$tTH2-mediated immunity protects against helminth infections --$tSummary to Chapter 10 --$tQuestions --$gch. 11$tImmunological Memory and Vaccination --$tImmunological memory and the secondary immune response --$g11-1.$tAntibodies made in a primary immune response persist for several months and provide protection --$g11-2.$tLow levels of pathogen-specific antibodies are maintained by long-lived plasma cells --$g11-3.$tLong-lived clones of memory B cells and T cells are produced in the primary immune response --$g11-4.$tMemory B cells and T cells provide protection against pathogens for decades and even for life --$g11-5.$tMaintaining populations of memory cells does not depend upon the persistence of antigen --$g11-6.$tChanges to the antigen receptor distinguish naive, effector, and memory B cells --$g11-7.$tIn the secondary immune response, memory B cells are activated whereas naive B cells are inhibited --$g11-8.$tActivation of the primary and secondary immune responses have common features --$g11-9.$tCombinations of cell-surface markers distinguish memory T cells from naive and effector T cells --$g11-10.$tCentral and effector memory T cells recognize pathogens in different tissues of the body --$g11-11.$tIn viral infections, numerous effector CD8 T cells give rise to relatively few memory T cells --$g11-12.$tImmune-complex-mediated inhibition of naive B cells is used to prevent hemolytic anemia of the newborn --$g11-13.$tIn the response to influenza virus, immunological memory is gradually eroded --$tSummary --$tVaccination to prevent infectious disease --$g11-14.$tProtection against smallpox is achieved by immunization with the less dangerous cowpox virus --
880 00 $6505-00/(S$aContents note continued:$tSummary --$tHematopoietic cell transplantation --$g15-20.$tHematopoietic cell transplantation is a treatment for genetic diseases of blood cells --$g15-21.$tAllogeneic hematopoietic cell transplantation is the preferred treatment for many cancers --$g15-22.$tAfter hematopoietic cell transplantation, the patient is attacked by alloreactive T cells in the graft --$g15-23.$tHLA matching of donor and recipient is most important for hematopoietic cell transplantation --$g15-24.$tMinor histocompatibility antigens trigger alloreactive T cells in recipients of HLA-identical transplants --$g15-25.$tSome GVHD helps engraftment and prevents relapse of malignant disease --$g15-26.$tNK cells also mediate graft-versus-leukemia effects --$g15-27.$tHematopoietic cell transplantation can induce tolerance of a solid organ transplant --$tSummary --$tSummary to Chapter 15 --$tQuestions --$gch. 16$tDisruption of Healthy Tissue by the Adaptive Immune Response --$g16-1.$tEvery autoimmune disease resembles a type II, III, or IV hypersensitivity reaction --$g16-2.$tAutoimmune diseases arise when tolerance to self antigens is lost --$g16-3.$tHLA is the dominant genetic factor affecting susceptibility to autoimmune disease --$g16-4.$tHLA associations reflect the importance of T-cell tolerance in preventing autoimmunity --$g16-5.$tBinding of antibodies to cell-surface receptors causes several autoimmune diseases --$g16-6.$tOrganized lymphoid tissue sometimes forms at sites inflamed by autoimmune disease --$g16-7.$tantibody response to an autoantigen can broaden and strengthen by epitope spreading --$g16-8.$tIntermolecular epitope spreading occurs in systemic autoimmune disease --$g16-9.$tIntravenous immunoglobulin is a therapy for autoimmune diseases --$g16-10.$tMonoclonal antibodies that target TNF-α and B cells are used to treat rheumatoid arthritis --$g16-11.$tRheumatoid arthritis is influenced by genetic and environmental factors --$g16-12.$tAutoimmune disease can be an adverse side-effect of an immune response to infection --$g16-13.$tNoninfectious environmental factors affect the development of autoimmune disease --$g16-14.$tType 1 diabetes is caused by the selective destruction of insulin-producing cells in the pancreas --$g16-15.$tCombinations of HLA class II allotypes confer susceptibility and resistance to type 1 diabetes --$g16-16.$tCeliac disease is a hypersensitivity to food that has much in common with autoimmune disease --$g16-17.$tCeliac disease is caused by the selective destruction of intestinal epithelial cells --$g16-18.$tSenescence of the thymus and the T-cell population contributes to autoimmunity --$g16-19.$tAutoinflammatory diseases of innate immunity --$tSummary to Chapter 16 --$tQuestions --$gch. 17$tCancer and Its Interactions With the Immune System --$g17-1.$tCancer results from mutations that cause uncontrolled cell growth --$g17-2.$tcancer arises from a single cell that has accumulated multiple mutations --$g17-3.$tExposure to chemicals, radiation, and viruses facilitates progression to cancer --$g17-4.$tCertain common features distinguish cancer cells from normal cells --$g17-5.$tImmune responses to cancer have similarities with those to virus-infected cells --$g17-6.$tAllogeneic differences in MHC class I molecules enable cytotoxic T cells to eliminate tumor cells --$g17-7.$tMutations acquired by somatic cells during oncogenesis can give rise to tumor-specific antigens --$g17-8.$tCancer/testis antigens are a prominent type of tumor-associated antigen --$g17-9.$tSuccessful tumors evade and manipulate the immune response --$g17-10.$tVaccination against human papillomaviruses can prevent cervical and other genital cancers --$g17-11.$tVaccination with tumor antigens can cause cancer to regress but it is unpredictable --$g17-12.$tMonoclonal antibodies that interfere with negative regulators of the immune response can be used to treat cancer --$g17-13.$tT-cell responses to tumor cells can be improved with chimeric antigen receptors --$g17-14.$tantitumor response of γ:δ T cells and NK cells can be augmented --$g17-15.$tT-cell responses to tumors can be improved by adoptive transfer of antigen-activated dendritic cells --$g17-16.$tMonoclonal antibodies are valuable tools for the diagnosis of cancer --$g17-17.$tMonoclonal antibodies against cell-surface antigens are increasingly used in cancer therapy --$tSummary to Chapter 17.
880 00 $6505-00/(S$aMachine generated contents note:$gch. 1$tElements of the Immune System and their Roles in Defense --$g1-1.$tNumerous commensal microorganisms inhabit healthy human bodies --$g1-2.$tPathogens are infectious organisms that cause disease --$g1-3.$tskin and mucosal surfaces form barriers against infection --$g1-4.$tinnate immune response causes inflammation at sites of infection --$g1-5.$tadaptive immune response adds to an ongoing innate immune response --$g1-6.$tAdaptive immunity is better understood than innate immunity --$g1-7.$tImmune system cells with different functions all derive from hematopoietic stem cells --$g1-8.$tImmunoglobulins and T-cell receptors are the diverse lymphocyte receptors of adaptive immunity --$g1-9.$tOn encountering their specific antigen, B cells and T cells differentiate into effector cells --$g1-10.$tAntibodies bind to pathogens and cause their inactivation or destruction --$g1-11.$tMost lymphocytes are present in specialized lymphoid tissues --$g1-12.$tAdaptive immunity is initiated in secondary lymphoid tissues --$g1-13.$tspleen provides adaptive immunity to blood infections --$g1-14.$tMost secondary lymphoid tissue is associated with the gut --$tSummary to Chapter 1 --$tQuestions --$gch. 2$tInnate Immunity: the Immediate Response to Infection --$g2-1.$tPhysical barriers colonized by commensal microorganisms protect against infection by pathogens --$g2-2.$tIntracellular and extracellular pathogens require different types of immune response --$g2-3.$tComplement is a system of plasma proteins that mark pathogens for destruction --$g2-4.$tAt the start of an infection, complement activation proceeds by the alternative pathway --$g2-5.$tRegulatory proteins determine the extent and site of C3b deposition --$g2-6.$tPhagocytosis by macrophages provides a first line of cellular defense against invading microorganisms --$g2-7.$tterminal complement proteins lyse pathogens by forming membrane pores --$g2-8.$tSmall peptides released during complement activation induce local inflammation --$g2-9.$tSeveral classes of plasma protein limit the spread of infection --$g2-10.$tAntimicrobial peptides kill pathogens by perturbing their membranes --$g2-11.$tPentraxins are plasma proteins of innate immunity that bind microorganisms and target them to phagocytes --$tSummary to Chapter 2 --$tQuestions --$gch. 3$tInnate Immunity: the Induced Response to Infection --$g3-1.$tCellular receptors of innate immunity distinguish 'non-self from 'self --$g3-2.$tTissue macrophages carry a battery of phagocytic and signaling receptors --$g3-3.$tRecognition of LPS by TLR4 induces changes in macrophage gene expression --$g3-4.$tActivation of resident macrophages induces a state of inflammation at sites of infection --$g3-5.$tNOD-like receptors recognize bacterial degradation products in the cytoplasm --$g3-6.$tInflammasomes amplify the innate immune response by increasing the production of IL-1β --$g3-7.$tNeutrophils are dedicated phagocytes and the first effector cells recruited to sites of infection --$g3-8.$tInflammatory cytokines recruit neutrophils from the blood to the infected tissue --$g3-9.$tNeutrophils are potent killers of pathogens and are themselves programmed to die --$g3-10.$tInflammatory cytokines raise body temperature and activate the liver to make the acute-phase response --$g3-11.$tlectin pathway of complement activation is initiated by the mannose-binding lectin --$g3-12.$tC-reactive protein triggers the classical pathway of complement activation --$g3-13.$tToll-like receptors sense the presence of the four main groups of pathogenic microorganisms --$g3-14.$tGenetic variation in Toll-like receptors is associated with resistance and susceptibility to disease --$g3-15.$tInternal detection of viral infection induces cells to make an interferon response --$g3-16.$tPlasmacytoid dendritic cells are factories for making large quantities of type I interferons --$g3-17.$tNatural killer cells are the main circulating lymphocytes that contribute to the innate immune response --$g3-18.$tTwo subpopulations of NK cells are differentially distributed in blood and tissues --$g3-19.$tNK-cell cytotoxicity is activated at sites of virus infection --$g3-20.$tNK cells and macrophages activate each other at sites of infection --$g3-21.$tInteractions between dendritic cells and NK cells influence the immune response --$tSummary to Chapter 3 --$tQuestions --$gch. 4$tAntibody Structure and the Generation of B-Cell Diversity --$tstructural basis of antibody diversity --$g4-1.$tAntibodies are composed of polypeptides with variable and constant regions --$g4-2.$tImmunoglobulin chains are folded into compact and stable protein domains --$g4-3.$tantigen-binding site is formed from the hypervariable regions of a heavy-chain V domain and a light-chain V domain --$g4-4.$tAntigen-binding sites vary in shape and physical properties --$g4-5.$tMonoclonal antibodies are produced from a clone of antibody-producing cells --$g4-6.$tMonoclonal antibodies are used as treatments for a variety of diseases --$tSummary --$tGeneration of immunoglobulin diversity in B cells before encounter with antigen --$g4-7.$tDNA sequence encoding a V region is assembled from two or three gene segments --$g4-8.$tRandom recombination of gene segments produces diversity in the antigen-binding sites of immunoglobulins --$g4-9.$tRecombination enzymes produce additional diversity in the antigen-binding site --$g4-10.$tDeveloping and naive B cells use alternative mRNA splicing to make both IgM and IgD --$g4-11.$tEach B cell produces immunoglobulin of a single antigen specificity --$g4-12.$tImmunoglobulin is first made in a membrane-bound form that is present on the B-cell surface --$tSummary --$tDiversification of antibodies after B cells encounter antigen --$g4-13.$tSecreted antibodies are produced by an alternative pattern of heavy-chain RNA processing --$g4-14.$tRearranged V-region sequences are further diversified by somatic hypermutation --$g4-15.$tIsotype switching produces immunoglobulins with different C regions but identical antigen specificities --$g4-16.$tAntibodies with different C regions have different effector functions --$g4-17.$tfour subclasses of IgG have different and complementary functions --$tSummary --$tSummary to Chapter 4 --$tQuestions --$gch. 5$tAntigen Recognition by T Lymphocytes --$tT-cell receptor diversity --$g5-1.$tT-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin --$g5-2.$tT-cell receptor diversity is generated by gene rearrangement --$g5-3.$tRAG genes were key elements in the origin of adaptive immunity --$g5-4.$tExpression of the T-cell receptor on the cell surface requires association with additional proteins --$g5-5.$tdistinct population of T cells expresses a second class of T-cell receptor with γ and δ chains --$tSummary --$tAntigen processing and presentation --$g5-6.$tT-cell receptors recognize peptide antigens bound to MHC molecules --$g5-7.$tTwo classes of MHC molecule present peptide antigens to two types of T cell --$g5-8.$ttwo classes of MHC molecule have similar three-dimensional structures --$g5-9.$tMHC molecules bind a variety of peptides --$g5-10.$tMHC class I and MHC class II molecules function in different intracellular compartments --$g5-11.$tPeptides generated in the cytosol are transported to the endoplasmic reticulum for binding to MHC class I molecules --$g5-12.$tMHC class I molecules bind peptides as part of a peptide-loading complex --$g5-13.$tPeptides presented by MHC class II molecules are generated in acidified intracellular vesicles --$g5-14.$tInvariant chain prevents MHC class II molecules from binding peptides in the endoplasmic reticulum --$g5-15.$tCross-presentation enables extracellular antigens to be presented by MHC class I --$g5-16.$tMHC class I molecules are expressed by most cell types, MHC class II molecules are expressed by few cell types --$g5-17.$tT-cell receptor specifically recognizes both peptide and MHC molecule --$tSummary --$tmajor histocompatibility complex --$g5-18.$tdiversity of MHC molecules in the human population is due to multigene families and genetic polymorphism --$g5-19.$tHLA class I and class II genes occupy different regions of the HLA complex --$g5-20.$tOther proteins involved in antigen processing and presentation are encoded in the HLA class II region --$g5-21.$tMHC polymorphism affects the binding of peptide antigens and their presentation to T cells --$g5-22.$tMHC diversity results from selection by infectious disease --$g5-23.$tMHC polymorphism triggers T-cell reactions that can reject transplanted organs --$tSummary --$tSummary to Chapter 5 --$tQuestions --$gch. 6$tDevelopment of B Lymphocytes --$tdevelopment of B cells in the bone marrow --$g6-1.$tB-cell development in the bone marrow proceeds through several stages --$g6-2.$tB-cell development is stimulated by bone marrow stromal cells --$g6-3.$tPro-B-cell rearrangement of the heavy-chain locus is an inefficient process --$g6-4.$tpre-B-cell receptor monitors the quality of immunoglobulin heavy chains --$g6-5.$tpre-B-cell receptor causes allelic exclusion at the immunoglobulin heavy-chain locus --$g6-6.$tRearrangement of the light-chain loci by pre-B cells is relatively efficient --$g6-7.$tDeveloping B cells pass two checkpoints in the bone marrow --$g6-8.$tprogram of protein expression underlies the stages of B-cell development --$g6-9.$tMany B-cell tumors carry chromosomal translocations that join immunoglobulin genes to genes that regulate cell growth --$g6-10.$tB cells expressing the glycoprotein CD5 express a distinctive repertoire of receptors --$tSummary --$tSelection and further development of the B-cell repertoire --$g6-11.$tpopulation of immature B cells is purged of cells bearing self-reactive B-cell receptors --
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