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Chapter 1 Elements of the Immune System and Their Roles in Defense |
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1 | (34) |
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1-1 Numerous commensal microorganisms inhabit healthy human bodies |
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5 | (1) |
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1-2 Pathogens are infectious organisms that cause disease |
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6 | (2) |
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1-3 Skin and mucosal surfaces are barrier defenses against infection |
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8 | (2) |
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1-4 The innate immune response produces a state of inflammation at sites of infection |
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10 | (2) |
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1-5 The adaptive immune response builds on the innate immune response |
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12 | (2) |
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1-6 Immune-system cells with different functions derive from hematopoietic stem cells |
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14 | (5) |
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1-7 Immunoglobulins and T-cell receptors are the antigen receptors of adaptive immunity |
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19 | (1) |
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1-8 On binding specific antigen, B cells and T cells divide and differentiate into effector cells |
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20 | (1) |
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1-9 B cells and T cells recognize different categories of microbial antigens |
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21 | (1) |
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1-10 Antibodies binding to a pathogen cause its inactivation or elimination |
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22 | (1) |
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1-11 Most lymphocytes are present in specialized lymphoid tissues |
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23 | (3) |
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1-12 Adaptive immunity is initiated in secondary lymphoid tissues |
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26 | (2) |
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1-13 The spleen provides adaptive immunity to blood infections |
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28 | (1) |
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1-14 Most of the body's secondary lymphoid tissue is associated with the gut |
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29 | (6) |
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30 | (1) |
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31 | (4) |
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Chapter 2 Innate Immunity: the Immediate Response to Infection |
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35 | (18) |
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2-1 Physical barriers colonized by commensal microorganisms protect against infection by pathogens |
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35 | (1) |
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2-2 Different immune responses are targeted to extracellular and intracellular infections |
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36 | (1) |
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2-3 Complement is a system of plasma proteins that mark pathogens for destruction |
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37 | (1) |
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2-4 At the start of an infection, complement activation proceeds by the alternative pathway |
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38 | (2) |
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2-5 Regulatory proteins determine the extent and site of C3b deposition |
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40 | (2) |
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2-6 The macrophage is a first line of cellular defense against an invading microorganism |
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42 | (1) |
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2-7 The terminal complement components make pores in microbial membranes |
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43 | (2) |
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2-8 Small peptides released during complement activation induce local inflammation |
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45 | (1) |
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2-9 Several systems of plasma proteins limit the spread of infection |
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46 | (1) |
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2-10 Defensins are antimicrobial peptides that kill pathogens by disrupting their membranes |
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47 | (1) |
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2-11 Pentraxins are plasma proteins that bind microorganisms and deliver them to phagocytes |
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48 | (5) |
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49 | (1) |
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49 | (4) |
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Chapter 3 Innate Immunity: the Induced Response to Infection |
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53 | (44) |
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Inflammation, innate immunity, and myeloid cells |
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53 | (1) |
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3-1 The receptors of innate immunity distinguish `self' from `non-self' and `altered-self' |
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54 | (2) |
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3-2 Tissue-resident macrophages use a multiplicity of surface receptors to detect infection |
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56 | (3) |
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3-3 Toll-like receptor 4 recognizes the lipopolysaccharide of Gram-negative bacteria |
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59 | (3) |
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3-4 Toll-like receptors sense the presence of the four main groups of pathogenic microorganisms |
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62 | (1) |
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3-5 TLR4 polymorphism influences disease susceptibility |
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63 | (1) |
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3-6 Intracellular NOD proteins recognize bacterial degradation products in the cytoplasm |
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63 | (1) |
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3-7 Cells infected with a virus make an interferon response |
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64 | (3) |
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3-8 Plasmacytoid dendritic cells specialize in the production of type I interferons |
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67 | (1) |
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3-9 Inflammasomes enable activated macrophages to release a large burst of IL-1β |
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67 | (3) |
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3-10 IL-α and IL-1β are members of a diverse and highly conserved cytokine family |
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70 | (1) |
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3-11 Autoinflammatory diseases arise from innate immune responses that attack self |
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70 | (2) |
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3-12 Inflammation of an infected tissue attracts blood-borne immune effector cells |
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72 | (1) |
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3-13 Recruitment of neutrophils from blood to tissue is mediated by adhesion molecules |
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73 | (2) |
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3-14 Neutrophils are potent killers of pathogens and are programmed to die |
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75 | (3) |
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3-15 Inflammatory cytokines cause fever and induce the acute-phase response by the liver |
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78 | (2) |
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3-16 The lectin pathway of complement activation is initiated by the mannose-binding lectin |
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80 | (2) |
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3-17 C-reactive protein triggers the classical pathway of complement activation |
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82 | (2) |
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83 | (1) |
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Inflammation, innate immunity, and lymphoid cells |
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84 | (1) |
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3-18 Five types of innate lymphoid cell contribute to inflammation and innate immunity |
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84 | (1) |
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3-19 The five types of innate lymphoid cell derive from a common innate lymphocyte precursor |
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85 | (1) |
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3-20 NK cells are circulating lymphocytes of the innate immune response |
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86 | (1) |
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3-21 Two subpopulations of NK cells are differentially distributed in blood and tissues |
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86 | (1) |
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3-22 NK-cell cytotoxicity is activated at sites of virus infection |
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87 | (2) |
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3-23 NK cells and macrophages activate each other at sites of infection |
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89 | (1) |
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3-24 Interactions between dendritic cells and NK cells influence the immune response |
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90 | (2) |
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3-25 The NK-cell population retains a memory of its encounters with pathogens |
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92 | (5) |
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92 | (1) |
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93 | (1) |
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94 | (3) |
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Chapter 4 Antibody Structure and the Generation of B-Cell Diversity |
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97 | (32) |
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The structural basis of antibody diversity |
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98 | (1) |
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4-1 Antibodies are composed of polypeptides with variable and constant regions |
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98 | (1) |
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4-2 Immunoglobulin chains are folded into compact and stable protein domains |
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99 | (2) |
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4-3 The antigen-binding site of an antibody is formed from the hypervariable regions of the heavy- and light-chain V domains |
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101 | (1) |
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4-4 Antigen-binding sites vary in shape and physical properties |
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102 | (1) |
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4-5 A monoclonal antibody is produced by a clone of antibody-producing cells |
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103 | (3) |
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4-6 Monoclonal antibodies are used as treatments for a variety of diseases |
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106 | (2) |
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107 | (1) |
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Generation of immunoglobulin diversity in B cells before encounter with antigen |
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107 | (1) |
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4-7 The DNA sequence encoding a V region is assembled from two or three gene segments |
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108 | (1) |
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4-8 Random recombination of gene segments creates diversity in the antigen-binding sites of immunoglobulins |
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109 | (2) |
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4-9 Recombination enzymes produce additional diversity in the antigen-binding site |
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111 | (1) |
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4-10 In naive B cells alternative mRNA splicing produces IgM and IgD of the same antigen specificity |
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112 | (1) |
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4-11 Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface |
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113 | (1) |
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114 | (1) |
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Diversification of antibodies after B cells encounter antigen |
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114 | (1) |
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4-12 Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing |
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114 | (1) |
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4-13 Rearranged V-region sequences are further diversified by somatic hypermutation |
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115 | (1) |
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4-14 Isotype switching produces immunoglobulin with a different constant region but identical antigen specificity |
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116 | (2) |
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4-15 Antibodies with different constant regions have different effector functions |
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118 | (2) |
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4-16 The four subclasses of IgG have different and complementary functions |
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120 | (9) |
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123 | (1) |
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123 | (3) |
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126 | (3) |
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Chapter 5 Antigen Recognition by T Lymphocytes |
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129 | (34) |
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T-cell receptor diversity |
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130 | (1) |
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5-1 The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin |
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130 | (1) |
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5-2 T-cell receptor diversity is generated by gene rearrangement |
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131 | (1) |
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5-3 Expression of the T-cell receptor on the T-cell surface requires association with additional proteins |
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132 | (1) |
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5-4 A distinctive population of T cells expresses a second class of T-cell receptor with γ and δ chains |
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133 | (2) |
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134 | (1) |
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Antigen processing and presentation |
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134 | (1) |
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5-5 T-cell receptors recognize peptide antigens bound to MHC molecules |
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135 | (1) |
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5-6 Two classes of MHC molecule present peptide antigens to two types of T cell |
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136 | (1) |
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5-7 MHC class I and class II molecules have similar structures |
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137 | (2) |
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5-8 MHC class I binds shorter and more precisely defined peptides than MHC class II |
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139 | (1) |
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5-9 MHC class I and class II bind peptides in different intracellular compartments |
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140 | (2) |
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5-10 Peptides produced in the cytosol are transported to the endoplasmic reticulum for binding to MHC class I |
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142 | (2) |
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5-11 MHC class I binds peptides in the context of a highly specific peptide-loading complex |
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144 | (1) |
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5-12 All cells express MHC class I, whereas MHC class II is mainly expressed by professional antigen-presenting cells |
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145 | (2) |
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5-13 Invariant chain prevents MHC class II from binding peptides in the endoplasmic reticulum |
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147 | (2) |
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5-14 Cross-presentation enables extracellular antigens to be presented by MHC class I |
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149 | (2) |
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150 | (1) |
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The major histocompatibility complex |
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150 | (1) |
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5-15 Human MHC diversity is the product of gene families and genetic polymorphisms |
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151 | (1) |
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5-16 HLA class I and class II genes occupy separate regions of the HLA complex |
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152 | (2) |
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5-17 Proteins involved in antigen processing and presentation are encoded by genes in the HLA class II region |
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154 | (1) |
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5-18 Some MHC class I and class II genes are highly polymorphic |
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155 | (1) |
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5-19 Selection by infectious disease is a likely major cause of HLA class I and class II diversity |
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156 | (1) |
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5-20 Human populations all maintain a diversity of HLA class I and class II alleles |
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157 | (6) |
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158 | (1) |
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159 | (1) |
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159 | (4) |
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Chapter 6 The Development of B Lymphocytes |
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163 | (28) |
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The development of B cells in the bone marrow |
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164 | (1) |
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6-1 B-cell development in the bone marrow proceeds through several stages |
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164 | (1) |
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6-2 B-cell development is stimulated by bone marrow stromal cells |
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165 | (1) |
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6-3 Rearrangement of the immunoglobulin heavy-chain genes occurs in pro-B cells |
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166 | (1) |
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6-4 The pre-B-cell receptor monitors the quality of immunoglobulin heavy chains |
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167 | (1) |
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6-5 Rearrangement of the light-chain loci occurs in pre-B cells |
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168 | (2) |
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6-6 B cells encounter two checkpoints during their development in the bone marrow |
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170 | (1) |
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6-7 A program of protein expression underlies the stages of B-cell development |
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171 | (3) |
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6-8 Many B-cell tumors have chromosomal translocations involving immunoglobulin genes |
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174 | (1) |
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6-9 B cells expressing the cell-surface protein CD5 have a distinctive repertoire of receptors |
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175 | (2) |
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176 | (1) |
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Selection and further development of the B-cell repertoire |
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177 | (1) |
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6-10 The immature B-cell population is purged of cells bearing self-reactive B-cell receptors |
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177 | (1) |
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6-11 The antigen receptors of autoreactive immature B cells can be modified by receptor editing |
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178 | (1) |
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6-12 Immature B cells that recognize monovalent self antigens are made nonresponsive |
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179 | (1) |
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6-13 Maturation and survival of B cells occurs in lymphoid follicles |
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180 | (2) |
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6-14 Encounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells |
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182 | (1) |
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6-15 Different types of B-cell tumor reflect B cells at different stages of development |
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183 | (8) |
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184 | (1) |
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185 | (2) |
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187 | (4) |
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Chapter 7 The Development of T Lymphocytes |
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191 | (22) |
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The development of T cells in the thymus |
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191 | (1) |
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7-1 T cells develop in the thymus |
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192 | (2) |
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7-2 Thymocytes commit to the T-cell lineage before rearranging their T-cell receptor genes |
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194 | (1) |
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7-3 The two lineages of T cells arise from a common thymocyte progenitor |
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195 | (2) |
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7-4 Gene rearrangement in double-negative thymocytes leads to assembly of either a γδ receptor or a pre-T-cell receptor |
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197 | (2) |
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7-5 Rearrangement of the α-chain gene occurs only in pre-T cells |
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199 | (1) |
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7-6 Stages in T-cell development are marked by changes in gene expression |
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200 | (3) |
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202 | (1) |
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Positive and negative selection of the T-cell repertoire |
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202 | (1) |
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7-7 T cells that recognize self-MHC molecules undergo positive selection in the thymus |
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203 | (1) |
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7-8 Positive selection is affected by peptides produced by a thymus-specific proteasome |
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204 | (1) |
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7-9 Continuing a-chain gene rearrangement increases the chance of positive selection |
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204 | (1) |
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7-10 Positive selection determines expression of either CD4 or CD8 |
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205 | (1) |
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7-11 T cells specific for self antigens are removed in the thymus by negative selection |
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206 | (1) |
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7-12 Tissue-specific proteins are expressed in the thymus and participate in negative selection |
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207 | (1) |
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7-13 Regulatory CD4 T cells comprise a distinct lineage of CD4 T cells |
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207 | (1) |
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7-14 T cells differentiate further after antigen recognition in secondary lymphoid tissue |
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207 | (6) |
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208 | (1) |
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208 | (2) |
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210 | (3) |
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Chapter 8 T Cell-Mediated Immunity |
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213 | (32) |
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Activation of naive T cells by antigen |
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213 | (1) |
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8-1 Dendritic cells carry antigens from sites of infection to secondary lymphoid tissues |
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214 | (2) |
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8-2 Dendritic cells are adept and versatile at processing pathogen antigens |
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216 | (1) |
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8-3 Naive T cells first encounter antigen presented by dendritic cells in secondary lymphoid tissues |
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217 | (1) |
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8-4 Homing of naive T cells to secondary lymphoid tissues is determined by chemokines and cell-adhesion molecules |
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218 | (2) |
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8-5 Activation of naive T cells requires signals from the antigen receptor and the co-stimulatory receptor |
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220 | (1) |
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8-6 Signals from T-cell receptors, co-receptors, and co-stimulatory receptors activate naive T cells |
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221 | (1) |
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8-7 Proliferation and differentiation of activated naive T cells are driven by the cytokine interleukin-2 |
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222 | (2) |
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8-8 Antigen recognition in the absence of co-stimulation leads to a state of T-cell anergy |
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224 | (1) |
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8-9 Activation of naive CD4 T cells gives rise to five types of effector CD4 T cell |
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225 | (1) |
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8-10 The cytokine environment determines which differentiation pathway a naive T cell takes |
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226 | (2) |
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8-11 Positive feedback in the cytokine environment can polarize the effector CD4 T-cell response |
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228 | (1) |
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8-12 Naive CD8 T cells require stronger activation than that for naive CD4 T cells |
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229 | (2) |
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230 | (1) |
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The properties and functions of effector T cells |
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231 | (1) |
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8-13 Cytotoxic CD8T cells and effector CD4 TH1, TH2, and TH17 cells work at sites of infection |
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231 | (1) |
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8-14 Effector T-cell functions are mediated by cytokines and cytotoxins |
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232 | (2) |
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8-15 Cytokines change the patterns of gene expression in the cells targeted by effector T cells |
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234 | (1) |
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8-16 Cytotoxic CD8 T cells are selective and serial killers of target cells at sites of infection |
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235 | (1) |
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8-17 Cytotoxic T cells kill their target cells by inducing apoptosis |
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236 | (1) |
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8-18 Effector TH1 CD4 cells induce macrophage activation |
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237 | (1) |
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8-19 Naive B cells and their helper TFH cells recognize different epitopes of the same antigen |
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238 | (1) |
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8-20 Treg cells limit the activities of effector CD4 and CD8T cells |
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239 | (6) |
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240 | (1) |
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240 | (1) |
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241 | (4) |
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Chapter 9 Immunity Mediated by B Cells and Antibodies |
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245 | (36) |
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Antibody production by B lymphocytes |
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245 | (1) |
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9-1 B-cell activation requires cross-linking of the B-cell receptor |
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246 | (1) |
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9-2 B-cell activation requires signals from the B-cell co-receptor |
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246 | (2) |
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9-3 Effective B cell-mediated immunity depends on help from CD4 TFH cells |
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248 | (1) |
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9-4 Follicular dendritic cells in the B-cell area store intact antigens and display them to B cells |
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249 | (1) |
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9-5 Antigen-activated B cells move close to the T-cell area to find a TFH cell |
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250 | (2) |
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9-6 The primary focus of clonal expansion in the medullary cords produces plasma cells secreting IgM |
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252 | (1) |
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9-7 Somatic hypermutation and isotype switching occur in the specialized microenvironment of the primary follicle |
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253 | (2) |
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9-8 Antigen-mediated selection of centrocytes drives affinity maturation of the B-cell response in the germinal center |
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255 | (2) |
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9-9 Cytokines made by TFH cells guide B-cell switching of immunoglobulin isotype |
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257 | (1) |
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9-10 TFH cells determine the differentiation of antigen-activated B cells into plasma cells or memory cells |
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257 | (2) |
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258 | (1) |
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Antibody effector functions |
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258 | (1) |
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9-11 IgM, IgG, and monomeric IgA protect the internal tissues of the body |
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259 | (1) |
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9-12 Dimeric IgA and pentameric IgM protect mucosal surfaces of the body |
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260 | (1) |
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9-13 IgE provides a mechanism for rapid ejection of parasites and pathogens from the body |
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261 | (3) |
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9-14 Before and after birth, mothers provide their children with protective antibodies |
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264 | (1) |
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9-15 High-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells |
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265 | (1) |
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9-16 High-affinity IgG and IgA antibodies neutralize microbial toxins and animal venoms |
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266 | (2) |
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9-17 Binding of IgM to antigen on a pathogen's surface activates complement by the classical pathway |
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268 | (1) |
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9-18 Two forms of C4 are fixed at different sites on pathogen surfaces |
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269 | (1) |
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9-19 Complement activation by IgG requires the participation of two or more IgG molecules |
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269 | (1) |
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9-20 Erythrocytes facilitate removal of immune complexes from the circulation |
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270 | (1) |
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9-21 Fey receptors enable effector cells to bind IgG and be activated by IgG bound to pathogens |
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271 | (2) |
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9-22 Several low-affinity Fc receptors are specific for IgG |
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273 | (1) |
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9-23 An Fc receptor acts as an antigen receptor for NK cells |
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274 | (1) |
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9-24 The Fc receptor for monomeric IgA 1 belongs to a different family than the Fc receptors for IgG and IgE |
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275 | (6) |
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275 | (2) |
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277 | (1) |
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277 | (4) |
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Chapter 10 Preventing Infection at Mucosal Surfaces |
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281 | (24) |
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10-1 The communication functions of mucosal surfaces render them vulnerable to infection |
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281 | (2) |
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10-2 Mucins are gigantic glycoproteins that endow the mucus with properties to protect epithelial surfaces |
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283 | (1) |
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10-3 Commensal microorganisms assist the gut in digesting food and maintaining health |
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283 | (3) |
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10-4 The gastrointestinal tract is invested with distinctive secondary lymphoid tissues |
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286 | (1) |
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10-5 Inflammation of mucosal tissues is associated with causation not cure of disease |
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287 | (2) |
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10-6 Intestinal epithelial cells contribute to innate immune responses in the gut |
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289 | (1) |
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10-7 Intestinal macrophages eliminate pathogens without creating a state of inflammation |
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290 | (1) |
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10-8 M cells transport microbes and antigens from the gut lumen to gut-associated lymphoid tissue |
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291 | (1) |
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10-9 Gut dendritic cells respond differently to food antigens, commensal microorganisms, and pathogens |
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291 | (2) |
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10-10 Activation of B cells and T cells in one mucosal tissue commits them to defending all mucosal tissues |
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293 | (1) |
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10-11 A variety of effector lymphocytes guard healthy mucosal tissue in the absence of infection |
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294 | (2) |
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10-12 B cells activated in mucosal tissues give rise to plasma cells secreting IgM and IgA at mucosal surfaces |
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296 | (1) |
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10-13 Secretory IgM and IgA protect mucosal surfaces from microbial invasion |
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297 | (1) |
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10-14 Two subclasses of IgA have complementary properties for controlling microbial populations |
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298 | (2) |
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10-15 People lacking IgA are able to survive, reproduce, and be generally healthy |
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300 | (5) |
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301 | (1) |
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302 | (3) |
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Chapter 11 Immunological Memory and Vaccination |
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305 | (34) |
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Immunological memory and the secondary immune response |
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306 | (1) |
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11-1 Immunological memory is essential for the survival of human populations |
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306 | (1) |
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11-2 Antibodies made in a primary response persist in the circulation to prevent reinfection |
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307 | (1) |
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11-3 Memory B cells, naive B cells, and plasma cells are distinguished by the expression of their B-cell receptors |
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308 | (1) |
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11-4 Immune complex-mediated inhibition of naive B cells is used to prevent hemolytic anemia of the newborn |
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309 | (1) |
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11-5 Long-lived plasma cells are the major mediators of B-cell memory |
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310 | (1) |
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11-6 In responses to influenza virus, immunological memory is gradually lost with successive infections |
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311 | (1) |
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11-7 Antigen-mediated activation of naive T cells gives rise to effector and memory T cells |
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312 | (2) |
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11-8 Two subpopulations of circulating memory cells patrol different tissues of the body |
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314 | (1) |
|
11-9 Primary infections of a non-lymphoid tissue produce resident memory T cells that live within the tissue |
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315 | (1) |
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11-10 Resident memory T cells are the most numerous type of memory T cell |
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316 | (1) |
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316 | (1) |
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Vaccination to prevent infectious disease |
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317 | (1) |
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11-11 Protection against smallpox is achieved by immunization with the less dangerous vaccinia virus |
|
|
317 | (1) |
|
11-12 Smallpox is the only infectious disease of humans that has been eradicated worldwide by vaccination |
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318 | (1) |
|
11-13 Most viral vaccines are made from killed or inactivated viruses |
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319 | (1) |
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11-14 Both inactivated and live-attenuated vaccines protect against poliovirus |
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320 | (1) |
|
11-15 Vaccination can inadvertently cause disease |
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321 | (1) |
|
11-16 Subunit vaccines are made from the most antigenic components of a pathogen |
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322 | (1) |
|
11-17 Invention and application of rotavirus vaccines took decades of research and development |
|
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322 | (1) |
|
11-18 Bacterial vaccines are made from whole bacteria, secreted toxins, or capsular polysaccharides |
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323 | (1) |
|
11-19 Conjugate vaccines enable high-affinity antibodies to be made against carbohydrate antigens |
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324 | (1) |
|
11-20 Adjuvants are added to vaccines to activate and enhance the immune response to a pathogen |
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325 | (1) |
|
11-21 Genome sequences of human pathogens have opened up new avenues for making vaccines |
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326 | (1) |
|
11-22 The rapidly evolving influenza virus requires continual vaccine development |
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327 | (3) |
|
11-23 The need for a vaccine and the demands placed upon it change with the prevalence of disease |
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330 | (1) |
|
11-24 Vaccines have yet to be made against pathogens that establish chronic infections |
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331 | (2) |
|
11-25 Vaccine development faces greater public scrutiny than does drug development |
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333 | (6) |
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334 | (1) |
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335 | (1) |
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|
335 | (4) |
|
Chapter 12 Coevolution of Innate and Adaptive Immunity |
|
|
339 | (36) |
|
Regulation of NK-cell function by MHC class I and related molecules |
|
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340 | (1) |
|
12-1 NK cells express a range of activating and inhibitory receptors |
|
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340 | (2) |
|
12-2 Fc receptor expression enables NK cells to participate in the adaptive immune response |
|
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342 | (1) |
|
12-3 A variety of NK-cell receptors recognize MHC class I and structurally related surface glycoproteins |
|
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343 | (2) |
|
12-4 Immunoglobulin-like NK-cell receptors recognize polymorphic epitopes of HLA-A, -B, and -C |
|
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345 | (1) |
|
12-5 NK cells are educated to detect pathological changes in MHC class I expression |
|
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346 | (3) |
|
12-6 Different genomic complexes encode lectin-like and immunoglobulin-like receptors for HLA class I |
|
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349 | (1) |
|
12-7 There are two distinctive forms of human KIR haplotypes |
|
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350 | (1) |
|
12-8 Cytomegalovirus infection induces proliferation of NK cells expressing the activating HLA-E receptor |
|
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351 | (1) |
|
12-9 Interactions of uterine NK cells with fetal MHC class I molecules affect reproductive success |
|
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352 | (5) |
|
|
|
355 | (1) |
|
Maintenance of tissue integrity by γδ T cells |
|
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356 | (1) |
|
12-10 γδ T cells are not subject to the same constraints as αβ T cells |
|
|
357 | (1) |
|
12-11 γδ T cells in blood and tissues express different yd receptors |
|
|
358 | (1) |
|
12-12 Vγ9:δ52 T cells respond to phosphoantigens bound by butyrophilins |
|
|
359 | (1) |
|
12-13 Vγ4:Vδ5 T cells detect both virus-infected cells and tumor cells |
|
|
360 | (1) |
|
12-14 γδ 8 T-cell receptors combine properties of the receptors of innate and adaptive immunity |
|
|
361 | (1) |
|
12-15 Vγ:Vδ1 T-cell receptors recognize lipid antigens presented by CD1d |
|
|
361 | (3) |
|
|
|
363 | (1) |
|
Restriction of αβ T cells by nonpolymorphic MHC class I---like molecules |
|
|
364 | (1) |
|
12-16 CD1-restricted αβ T cells recognize lipid antigens of mycobacteria |
|
|
364 | (1) |
|
12-17 NKT cells are innate lymphocytes with αβ T-cell receptors that recognize lipid antigens |
|
|
365 | (3) |
|
12-18 Mucosa-associated invariant T cells detect bacteria and fungi that make riboflavin |
|
|
368 | (7) |
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|
369 | (1) |
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|
370 | (1) |
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|
371 | (4) |
|
Chapter 13 Failures of the Body's Defenses |
|
|
375 | (36) |
|
Evasion and subversion of the immune system by pathogens |
|
|
375 | (1) |
|
13-1 Genetic variation within some species of pathogens prevents effective long-term immunity |
|
|
376 | (1) |
|
13-2 Mutation and recombination allow influenza virus to escape from immunity |
|
|
376 | (2) |
|
13-3 Trypanosomes use gene conversion to change their surface antigens |
|
|
378 | (1) |
|
13-4 Herpesviruses persist in human hosts by hiding from the immune response |
|
|
379 | (2) |
|
13-5 Human herpesviruses cause a variety of diseases |
|
|
381 | (1) |
|
13-6 Some bacteria and parasites subvert the human immune response |
|
|
382 | (1) |
|
13-7 Bacterial superantigens stimulate a massive 1 but ineffective CD4 T-cell response |
|
|
383 | (1) |
|
13-8 Subversion of IgA by bacterial IgA-binding proteins |
|
|
384 | (1) |
|
|
|
384 | (1) |
|
Inherited immunodeficiency diseases |
|
|
384 | (1) |
|
13-9 Rare primary immunodeficiency diseases reveal how the human immune system works |
|
|
385 | (2) |
|
13-10 Inherited immunodeficiency diseases are caused by dominant, recessive, or X-linked gene defects |
|
|
387 | (1) |
|
13-11 Recessive and dominant mutations in the IFN-y receptor cause immunodeficiency of differing severity |
|
|
387 | (1) |
|
13-12 Antibody deficiency leads to poor clearing of extracellular bacteria |
|
|
388 | (2) |
|
13-13 Diminished production of antibodies can arise from inherited defects in T-cell help |
|
|
390 | (1) |
|
13-14 Complement defects impair antibody-mediated immunity and cause immune-complex disease |
|
|
390 | (1) |
|
13-15 Defects in phagocytes cause enhanced susceptibility to bacterial infection |
|
|
391 | (1) |
|
13-16 Defects in T-cell function underlie severe combined immunodeficiencies |
|
|
392 | (2) |
|
13-17 Some inherited immunodeficiencies cause susceptibility to particular pathogens |
|
|
394 | (2) |
|
|
|
394 | (1) |
|
Acquired immune deficiency syndrome |
|
|
395 | (1) |
|
13-18 HIV is a retrovirus that causes a slowly progressing chronic disease |
|
|
396 | (1) |
|
13-19 Human immune systems are better adapted to HIV-2 than to HIV-1 |
|
|
396 | (1) |
|
13-20 HIV infects CD4 T cells, macrophages, and dendritic cells |
|
|
397 | (2) |
|
13-21 In the 20th century most HIV infections progressed to AIDS |
|
|
399 | (1) |
|
13-22 Genetic deficiency of the CCR5 co-receptor for HIV confers resistance to infection |
|
|
400 | (1) |
|
13-23 HLA and KIR polymorphisms influence progression to AIDS |
|
|
401 | (1) |
|
13-24 HIV resists the immune response and gains resistance to antiviral drugs through rapid mutation |
|
|
402 | (2) |
|
13-25 Clinical latency is a period of active infection and renewal of CD4 T cells |
|
|
404 | (1) |
|
13-26 HIV infection leads to immunodeficiency and death from opportunistic infections |
|
|
404 | (1) |
|
13-27 A minority of HIV-infected individuals make antibodies that neutralize many strains of HIV |
|
|
405 | (6) |
|
|
|
406 | (1) |
|
|
|
406 | (1) |
|
|
|
407 | (4) |
|
Chapter 14 Allergy and the Immune Response to Parasites |
|
|
411 | (28) |
|
14-1 Different effector mechanisms underlie the four types of hypersensitivity reaction |
|
|
411 | (3) |
|
Shared mechanisms of immunity and allergy |
|
|
413 | (1) |
|
14-2 Th2 immune responses defend the body against infestation with multicellular parasites |
|
|
414 | (1) |
|
14-3 Allergy prevails in the industrialized countries where parasite infections have been eradicated |
|
|
415 | (1) |
|
14-4 Basophils initiate the Th2 response |
|
|
416 | (1) |
|
14-5 IgE antibodies emerge at early and late times in the primary immune response |
|
|
416 | (1) |
|
14-6 IgE differs in structure and function from other immunoglobulin isotypes |
|
|
417 | (1) |
|
14-7 Together, IgE and FceRI arm each mast cell with a high diversity of antigen-specific receptors |
|
|
418 | (1) |
|
14-8 FceRII is expressed by B cells and regulates the production of IgE |
|
|
419 | (1) |
|
14-9 Allergic disease can be treated with an IgE-specific monoclonal antibody |
|
|
420 | (1) |
|
14-10 Mast cells defend and maintain the tissues in which they reside |
|
|
421 | (1) |
|
14-11 Mast cells in tissues orchestrate IgE-mediated reactions through the release of inflammatory mediators |
|
|
422 | (1) |
|
14-12 Eosinophils are specialized granulocytes that release toxic mediators in IgE-mediated immune responses |
|
|
423 | (2) |
|
|
|
424 | (1) |
|
IgE-mediated allergic disease |
|
|
425 | (1) |
|
14-13 Allergens are protein antigens that can resemble parasite antigens |
|
|
425 | (1) |
|
14-14 Predisposition to allergic disease is influenced by genetic and environmental factors |
|
|
426 | (1) |
|
14-15 IgE-mediated allergic reactions consist of an immediate response followed by a late-phase response |
|
|
427 | (1) |
|
14-16 The effects of IgE-mediated allergic reactions vary with the site of mast-cell activation |
|
|
428 | (1) |
|
14-17 Systemic anaphylaxis is caused by allergens in the blood |
|
|
429 | (2) |
|
14-18 Rhinitis and asthma are caused by inhaled allergens |
|
|
431 | (1) |
|
14-19 Urticaria and angioedema are allergic reactions in the skin |
|
|
432 | (1) |
|
14-20 Atopic dermatitis is a chronic disease affecting the skin that has multiple risk factors |
|
|
433 | (1) |
|
14-21 Food allergies cause systemic effects as well as gut reactions |
|
|
434 | (1) |
|
14-22 Allergic reactions are prevented and treated by three complementary approaches |
|
|
434 | (5) |
|
|
|
435 | (1) |
|
|
|
435 | (1) |
|
|
|
436 | (3) |
|
Chapter 15 Transplantation of Tissues and Organs |
|
|
439 | (36) |
|
Allogeneic transplantation can trigger hypersensitivity reactions |
|
|
439 | (1) |
|
15-1 Blood is the most commonly transplanted tissue |
|
|
440 | (1) |
|
15-2 Incompatibility of blood group antigens causes type II hypersensitivity reactions |
|
|
440 | (2) |
|
15-3 Hyperacute rejection of transplanted organs is a type II hypersensitivity reaction |
|
|
442 | (1) |
|
15-4 Anti-HLA antibodies arise from pregnancy, blood transfusion, and transplantation |
|
|
443 | (1) |
|
15-5 Acute transplant rejection and graft-versus-host disease are type IV hypersensitivity reactions |
|
|
443 | (2) |
|
|
|
445 | (1) |
|
Transplantation of solid organs |
|
|
445 | (1) |
|
15-6 Organ transplantation involves procedures that produce inflammation in the donated organ and the transplant recipient |
|
|
445 | (1) |
|
15-7 HLA differences between transplant donor and recipient activate numerous alloreactive T cells |
|
|
446 | (1) |
|
15-8 Acute rejection is a type IV hypersensitivity caused by T cells responding to HLA differences between donor and recipient |
|
|
447 | (1) |
|
15-9 Chronic rejection of transplanted organs is equivalent to a type III hypersensitivity reaction |
|
|
448 | (2) |
|
15-10 Matching donor and recipient HLA class I and class II allotypes improves the outcome of kidney transplantation |
|
|
450 | (1) |
|
15-11 Immunosuppressive drugs enable allogeneic kidney transplantation to be a routine therapy |
|
|
451 | (1) |
|
15-12 Immunosuppression is given before and after kidney transplantation |
|
|
452 | (1) |
|
15-13 T-cell activation by alloantigens can be specifically prevented by immunosuppressive drugs |
|
|
453 | (3) |
|
15-14 Blocking cytokine signaling prevents the activation of alloreactive T cells |
|
|
456 | (1) |
|
15-15 Cytotoxic drugs target the replication and proliferation of activated alloreactive T cells |
|
|
457 | (1) |
|
15-16 Patients needing a transplant outnumber the available organs |
|
|
458 | (1) |
|
15-17 The need for HLA matching and immunosuppressive therapy varies with the organ transplanted |
|
|
459 | (3) |
|
|
|
460 | (1) |
|
Hematopoietic cell transplantation |
|
|
461 | (1) |
|
15-18 Hematopoietic cell transplantation is a treatment for genetic diseases of blood cells |
|
|
462 | (2) |
|
15-19 Allogeneic hematopoietic cell transplantation is the preferred treatment for many cancers |
|
|
464 | (1) |
|
15-20 After hematopoietic cell transplantation, the patient is attacked by alloreactive T cells in the graft |
|
|
464 | (1) |
|
15-21 HLA matching of donor and recipient is most important for hematopoietic cell transplantation |
|
|
465 | (2) |
|
15-22 Minor histocompatibility antigens activate alloreactive T cells in recipients of HLA-identical transplants |
|
|
467 | (1) |
|
15-23 Some GVHD helps engraftment and prevents relapse of malignant disease |
|
|
467 | (1) |
|
15-24 NK cells mediate graft-versus-leukemia effects |
|
|
468 | (1) |
|
15-25 Hematopoietic cell transplantation can induce tolerance of a solid organ transplant |
|
|
469 | (6) |
|
|
|
470 | (1) |
|
|
|
470 | (1) |
|
|
|
471 | (4) |
|
Chapter 16 Disruption of Healthy Tissue by the Adaptive Immune Response |
|
|
475 | (32) |
|
16-1 Every autoimmune disease resembles a type II, III, or IV hypersensitivity reaction |
|
|
476 | (1) |
|
16-2 Autoimmune diseases arise when f tolerance to self antigens is lost |
|
|
477 | (1) |
|
16-3 Most autoimmune responses and diseases are initiated by autoreactive Th17 CD4T cells |
|
|
478 | (1) |
|
16-4 HLA is the dominant genetic factor affecting susceptibility to autoimmune disease |
|
|
479 | (2) |
|
16-5 Autoimmune disease is more prevalent in women than in men |
|
|
481 | (1) |
|
16-6 HLA associations reflect the importance of T-cell tolerance in preventing autoimmunity |
|
|
482 | (1) |
|
16-7 Binding of antibody to a cell-surface receptor can cause an autoimmune disease |
|
|
482 | (3) |
|
16-8 Tertiary lymphoid tissue forms in tissues inflamed by autoimmune disease |
|
|
485 | (1) |
|
16-9 The antibody response to an autoantigen can broaden and strengthen by epitope spreading |
|
|
486 | (2) |
|
16-10 Intermolecular epitope spreading occurs in systemic autoimmune disease |
|
|
488 | (1) |
|
16-11 Intravenous immunoglobulin is a therapy for autoimmune diseases |
|
|
489 | (2) |
|
16-12 Monoclonal antibodies that target TNF-α and B cells are used to treat rheumatoid arthritis |
|
|
491 | (1) |
|
16-13 Rheumatoid arthritis is associated with genetic and environmental factors |
|
|
492 | (2) |
|
16-14 An autoimmune disease caused by physical trauma |
|
|
494 | (1) |
|
16-15 Type 1 diabetes is caused by selective destruction of insulin-producing cells of the pancreas |
|
|
495 | (1) |
|
16-16 Combinations of HLA class II allotypes confer susceptibility and resistance to type 1 diabetes |
|
|
496 | (2) |
|
16-17 Celiac disease is a hypersensitivity to food that has much in common with autoimmune disease |
|
|
498 | (1) |
|
16-18 Celiac disease is caused by the selective destruction of intestinal epithelial cells |
|
|
498 | (3) |
|
16-19 Senescence of the thymus and the T-cell population contributes to autoimmunity |
|
|
501 | (6) |
|
|
|
502 | (1) |
|
|
|
503 | (4) |
|
Chapter 17 Cancer, Immunity, and Immunotherapy |
|
|
507 | |
|
The evolution of cancer from healthy human cells |
|
|
508 | (1) |
|
17-1 Cancer results from mutations that cause uncontrolled cell growth |
|
|
508 | (1) |
|
17-2 Cancer arises from a cell that has accumulated multiple mutations |
|
|
509 | (1) |
|
17-3 Exposure to chemicals, radiation, and viruses facilitates progression to cancer |
|
|
510 | (1) |
|
17-4 Common features of cancer cells distinguish them from normal cells |
|
|
511 | (1) |
|
Human immune responses to cancer |
|
|
511 | (1) |
|
17-5 Immune responses to cancer have similarities to those made against virus-infected cells |
|
|
512 | (1) |
|
17-6 Mutations acquired by somatic cells during oncogenesis give rise to tumor-specific antigens |
|
|
513 | (1) |
|
17-7 Cancer/testis antigens are a prominent class of tumor-associated antigen |
|
|
514 | (1) |
|
17-8 Control of cancer by the immune system does not require elimination of all the tumor cells |
|
|
515 | (1) |
|
17-9 Successful tumors are ones that evade and manipulate the immune response |
|
|
515 | (2) |
|
17-10 Vaccination against human papillomavirus antigens prevents the occurrence of genital cancers |
|
|
517 | (1) |
|
Controlling cancer with immunotherapy |
|
|
518 | (1) |
|
17-11 Monoclonal antibodies are valuable tools for the diagnosis of cancer |
|
|
518 | (3) |
|
17-12 Monoclonal antibodies against cell-surface antigens are increasingly used in cancer immunotherapy |
|
|
521 | (1) |
|
17-13 Monoclonal antibodies specific for inhibitory regulators of T-cell responses are effective therapies for cancer |
|
|
522 | (1) |
|
17-14 Adoptive cell transfer improves the natural T-cell response to a tumor |
|
|
523 | (2) |
|
17-15 T-cell responses to tumor cells can be improved using chimeric antigen receptors |
|
|
525 | (1) |
|
17-16 T-cell responses to tumors can be improved by adoptive transfer of antigen-activated dendritic cells |
|
|
526 | |
|
|
|
527 | (1) |
|
|
|
528 | |
|
|
|
1 | (1) |
| Glossary |
|
1 | (1) |
| Credits |
|
1 | (1) |
| Index |
|
1 | |
