The immune system /

"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,...

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Bibliographic Details
Main Author:	Parham, Peter, 1950- (Author, http://id.loc.gov/vocabulary/relators/aut)
Corporate Author:	Clarence J. Marshall Memorial Library Fund
Format:	Book
Language:	English
Published:	New York, NY : W.W. Norton & Company, [2021]
Edition:	Fifth edition
Subjects:	Immune system Immunity Immunopathology Immune System Phenomena Immune System Immunité Immunopathologie Système immunitaire Textbooks

Table of 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: 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
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: 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

The immune system /

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