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Chapter 1 Elements of the Immune System and their Roles in Defense |
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1 | (28) |
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1-1 Numerous commensal microorganisms inhabit healthy human bodies |
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2 | (1) |
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1-2 Pathogens are infectious organisms that cause disease |
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3 | (1) |
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1-3 The skin and mucosal surfaces form barriers against infection |
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4 | (4) |
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1-4 The innate immune response causes inflammation at sites of infection |
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8 | (2) |
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1-5 The adaptive immune response adds to an ongoing innate immune response |
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10 | (2) |
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1-6 Adaptive immunity is better understood than innate immunity |
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12 | (1) |
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1-7 Immune system cells with different functions all derive from hematopoietic stem cells |
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12 | (4) |
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1-8 Immunoglobulins and T-cell receptors are the diverse lymphocyte receptors of adaptive immunity |
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16 | (1) |
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1-9 On encountering their specific antigen, B cells and T cells differentiate into effector cells |
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17 | (1) |
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1-10 Antibodies bind to pathogens and cause their inactivation or destruction |
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18 | (1) |
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1-11 Most lymphocytes are present in specialized lymphoid tissues |
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19 | (1) |
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1-12 Adaptive immunity is initiated in secondary lymphoid tissues |
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20 | (3) |
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1-13 The spleen provides adaptive immunity to blood infections |
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23 | (2) |
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1-14 Most secondary lymphoid tissue is associated with the gut |
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25 | (4) |
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26 | (1) |
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27 | (2) |
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Chapter 2 Innate Immunity: the Immediate Response to Infection |
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29 | (18) |
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2-1 Physical barriers colonized by commensal microorganisms protect against infection by pathogens |
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29 | (1) |
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2-2 Intracellular and extracellular pathogens require different types of immune response |
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30 | (1) |
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2-3 Complement is a system of plasma proteins that mark pathogens for destruction |
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31 | (1) |
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2-4 At the start of an infection, complement activation proceeds by the alternative pathway |
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32 | (2) |
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2-5 Regulatory proteins determine the extent and site of C3b deposition |
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34 | (2) |
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2-6 Phagocytosis by macrophages provides a first line of cellular defense against invading microorganisms |
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36 | (1) |
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2-7 The terminal complement proteins lyse pathogens by forming membrane pores |
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37 | (2) |
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2-8 Small peptides released during complement activation induce local inflammation |
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39 | (1) |
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2-9 Several classes of plasma protein limit the spread of infection |
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39 | (2) |
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2-10 Antimicrobial peptides kill pathogens by perturbing their membranes |
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41 | (2) |
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2-11 Pentraxins are plasma proteins of innate immunity that bind microorganisms and target them to phagocytes |
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43 | (4) |
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43 | (1) |
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44 | (3) |
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Chapter 3 Innate Immunity: the Induced Response to Infection |
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47 | (34) |
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3-1 Cellular receptors of innate immunity distinguish 'non-self from 'self |
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47 | (2) |
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3-2 Tissue macrophages carry a battery of phagocytic and signaling receptors |
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49 | (2) |
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3-3 Recognition of LPS by TLR4 induces changes in macrophage gene expression |
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51 | (2) |
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3-4 Activation of resident macrophages induces a state of inflammation at sites of infection |
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53 | (1) |
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3-5 NOD-like receptors recognize bacterial degradation products in the cytoplasm |
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54 | (1) |
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3-6 Inflammasomes amplify the innate immune response by increasing the production of 1L-1β |
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55 | (1) |
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3-7 Neutrophils are dedicated phagocytes and the first effector cells recruited to sites of infection |
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56 | (1) |
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3-8 Inflammatory cytokines recruit neutrophils from the blood to the infected tissue |
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57 | (2) |
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3-9 Neutrophils are potent killers of pathogens and are themselves programmed to die |
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59 | (3) |
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3-10 Inflammatory cytokines raise body temperature and activate the liver to make the acute-phase response |
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62 | (1) |
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3-11 The lectin pathway of complement activation is initiated by the mannose-binding lectin |
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63 | (3) |
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3-12 C-reactive protein triggers the classical pathway of complement activation |
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66 | (1) |
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3-13 Toll-like receptors sense the presence of the four main groups of pathogenic microorganisms |
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66 | (1) |
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3-14 Genetic variation in Toll-like receptors is associated with resistance and susceptibility to disease |
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67 | (1) |
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3-15 Internal detection of viral infection induces cells to make an interferon response |
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68 | (3) |
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3-16 Plasmacytoid dendritic cells are factories for making large quantities of type I interferons |
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71 | (1) |
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3-17 Natural killer cells are the main circulating lymphocytes that contribute to the innate immune response |
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71 | (1) |
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3-18 Two subpopulations of NK cells are differentially distributed in blood and tissues |
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72 | (1) |
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3-19 NK-cell cytotoxicity is activated at sites of virus infection |
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73 | (2) |
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3-20 NK cells and macrophages activate each other at sites of infection |
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75 | (1) |
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3-21 Interactions between dendritic cells and NK cells influence the immune response |
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76 | (5) |
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78 | (1) |
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78 | (3) |
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Chapter 4 Antibody Structure and the Generation of B-Cell Diversity |
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81 | (32) |
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The structural basis of antibody diversity |
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82 | (1) |
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4-1 Antibodies are composed of polypeptides with variable and constant regions |
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82 | (1) |
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4-2 Immunoglobulin chains are folded into compact and stable protein domains |
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83 | (2) |
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4-3 An antigen-binding site is formed from the hypervariable regions of a heavy-chain V domain and a light-chain V domain |
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85 | (1) |
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4-4 Antigen-binding sites vary in shape and physical properties |
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86 | (2) |
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4-5 Monoclonal antibodies are produced from a clone of antibody-producing cells |
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88 | (2) |
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4-6 Monoclonal antibodies are used as treatments for a variety of diseases |
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90 | (1) |
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91 | (1) |
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Generation of immunoglobulin diversity in B cells before encounter with antigen |
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91 | (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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91 | (1) |
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4-8 Random recombination of gene segments produces diversity in the antigen-binding sites of immunoglobulins |
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92 | (3) |
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4-9 Recombination enzymes produce additional diversity in the antigen-binding site |
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95 | (1) |
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4-10 Developing and naive B cells use alternative mRNA splicing to make both IgM and IgD |
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96 | (1) |
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4-11 Each B cell produces immunoglobulin of a single antigen specificity |
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96 | (1) |
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4-12 Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface |
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97 | (1) |
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98 | (1) |
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Diversification of antibodies after B cells encounter antigen |
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98 | (1) |
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4-13 Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing |
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98 | (2) |
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4-14 Rearranged V-region sequences are further diversified by somatic hypermutation |
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100 | (1) |
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4-15 Isotype switching produces immunoglobulins with different C regions but identical antigen specificities |
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101 | (2) |
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4-16 Antibodies with different C regions have different effector functions |
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103 | (2) |
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4-17 The four subclasses of IgG have different and complementary functions |
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105 | (8) |
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107 | (1) |
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107 | (3) |
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110 | (3) |
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Chapter 5 Antigen Recognition by T Lymphocytes |
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113 | (36) |
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T-cell receptor diversity |
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114 | (1) |
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5-1 The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin |
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114 | (1) |
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5-2 T-cell receptor diversity is generated by gene rearrangement |
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115 | (2) |
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5-3 The RAG genes were key elements in the origin of adaptive immunity |
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117 | (1) |
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5-4 Expression of the T-cell receptor on the cell surface requires association with additional proteins |
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117 | (1) |
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5-5 A distinct population of T cells expresses a second class of T-cell receptor with γ and δ chains |
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118 | (3) |
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119 | (1) |
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Antigen processing and presentation |
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120 | (1) |
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5-6 T-cell receptors recognize peptide antigens bound to MHC molecules |
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121 | (1) |
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5-7 Two classes of MHC molecule present peptide antigens to two types of T cell |
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122 | (1) |
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5-8 The two classes of MHC molecule have similar three-dimensional structures |
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123 | (1) |
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5-9 MHC molecules bind a variety of peptides |
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124 | (1) |
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5-10 MHC class I and MHC class II molecules function in different intracellular compartments |
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125 | (1) |
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5-11 Peptides generated in the cytosol are transported to the endoplasmic reticulum for binding to MHC class I molecules |
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126 | (1) |
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5-12 MHC class I molecules bind peptides as part of a peptide-loading complex |
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127 | (2) |
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5-13 Peptides presented by MHC class II molecules are generated in acidified intracellular vesicles |
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129 | (1) |
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5-14 Invariant chain prevents MHC class II molecules from binding peptides in the endoplasmic reticulum |
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130 | (1) |
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5-15 Cross-presentation enables extracellular antigens to be presented by MHC class I |
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131 | (1) |
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5-16 MHC class I molecules are expressed by most cell types, MHC class II molecules are expressed by few cell types |
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132 | (1) |
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5-17 The T-cell receptor specifically recognizes both peptide and MHC molecule |
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132 | (3) |
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133 | (2) |
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The major histocompatibility complex |
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135 | (1) |
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5-18 The diversity of MHC molecules in the human population is due to multigene families and genetic polymorphism |
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135 | (2) |
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5-19 The HLA class I and class II genes occupy different regions of the HLA complex |
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137 | (1) |
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5-20 Other proteins involved in antigen processing and presentation are encoded in the HLA class II region |
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138 | (1) |
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5-21 MHC polymorphism affects the binding of peptide antigens and their presentation to T cells |
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138 | (2) |
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5-22 MHC diversity results from selection by infectious disease |
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140 | (3) |
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5-23 MHC polymorphism triggers T-cell reactions that can reject transplanted organs |
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143 | (6) |
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144 | (1) |
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144 | (1) |
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145 | (4) |
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Chapter 6 The Development of B Lymphocytes |
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149 | (28) |
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The development of B cells in the bone marrow |
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150 | (1) |
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6-1 B-cell development in the bone marrow proceeds through several stages |
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150 | (1) |
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6-2 B-cell development is stimulated by bone marrow stromal cells |
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151 | (1) |
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6-3 Pro-B-cell rearrangement of the heavy-chain locus is an inefficient process |
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152 | (1) |
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6-4 The pre-B-cell receptor monitors the quality of immunoglobulin heavy chains |
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153 | (1) |
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6-5 The pre-B-cell receptor causes allelic exclusion at the immunoglobulin heavy-chain locus |
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154 | (1) |
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6-6 Rearrangement of the light-chain loci by pre-B cells is relatively efficient |
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155 | (2) |
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6-7 Developing B cells pass two checkpoints in the bone marrow |
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157 | (1) |
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6-8 A program of protein expression underlies the stages of B-cell development |
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157 | (3) |
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6-9 Many B-cell tumors carry chromosomal translocations that join immunoglobulin genes to genes that regulate cell growth |
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160 | (1) |
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6-10 B cells expressing the glycoprotein CD5 express a distinctive repertoire of receptors |
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161 | (3) |
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162 | (1) |
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Selection and further development of the B-cell repertoire |
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163 | (1) |
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6-11 The population of immature B cells is purged of cells bearing self-reactive B-cell receptors |
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164 | (1) |
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6-12 The antigen receptors of autoreactive immature B cells can be modified by receptor editing |
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165 | (1) |
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6-13 Immature B cells specific for monovalent self antigens are made nonresponsive to antigen |
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166 | (1) |
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6-14 Maturation and survival of B cells requires access to lymphoid follicles |
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167 | (1) |
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6-15 Encounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells |
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168 | (2) |
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6-16 Different types of B-cell tumor reflect B cells at different stages of development |
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170 | (7) |
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170 | (2) |
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172 | (1) |
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173 | (4) |
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Chapter 7 The Development of T Lymphocytes |
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177 | (22) |
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7-1 T cells develop in the thymus |
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178 | (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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180 | (1) |
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7-3 The two lineages of T cells arise from a common thymocyte progenitor |
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181 | (2) |
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7-4 Gene rearrangement in double-negative thymocytes leads to assembly of either a γ:δ receptor or a pre-T-cell receptor |
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183 | (1) |
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7-5 Thymocytes can make four attempts to rearrange a β-chain gene |
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184 | (1) |
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7-6 Rearrangement of the α-chain gene occurs only in pre-T cells |
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185 | (1) |
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7-7 Stages in T-cell development are marked by changes in gene expression |
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186 | (3) |
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188 | (1) |
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Positive and negative selection of the T-cell repertoire |
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188 | (1) |
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7-8 T cells that recognize self-MHC molecules are positively selected in the thymus |
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189 | (1) |
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7-9 Continuing α-chain gene rearrangement increases the chance for positive selection |
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190 | (1) |
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7-10 Positive selection determines expression of either the CD4 or the CD8 co-receptor |
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191 | (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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192 | (1) |
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7-12 Tissue-specific proteins are expressed in the thymus and participate in negative selection |
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192 | (1) |
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7-13 Regulatory CD4 T cells comprise a distinct lineage of CD4T cells |
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193 | (1) |
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7-14 T cells undergo further differentiation in secondary lymphoid tissues after encounter with antigen |
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193 | (6) |
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194 | (1) |
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194 | (2) |
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196 | (3) |
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Chapter 8 T Cell-Mediated Immunity |
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199 | (32) |
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Activation of naive T cells by antigen |
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199 | (1) |
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8-1 Dendritic cells carry antigens from sites of infection to secondary lymphoid tissues |
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200 | (2) |
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8-2 Dendritic cells are adept and versatile at processing pathogen antigens |
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202 | (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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203 | (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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204 | (2) |
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8-5 Activation of naive T cells requires signals from the antigen receptor and a co-stimulatory receptor |
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206 | (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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207 | (2) |
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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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209 | (1) |
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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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210 | (1) |
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8-9 Activation of naive CD4 T cells gives rise to effector CD4 T cells with distinctive helper functions |
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211 | (2) |
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8-10 The cytokine environment determines which differentiation pathway a naive T cell takes |
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213 | (1) |
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8-11 Positive feedback in the cytokine environment can polarize the effector CD4 T-cell response |
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214 | (1) |
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8-12 Naive CD8 T cells require stronger activation than naive CD4 T cells |
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215 | (3) |
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217 | (1) |
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The properties and functions of effector T cells |
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218 | (1) |
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8-13 Cytotoxic CD8 T cells and effector CD4 TH1, TH2, and TH17 work at sites of infection |
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218 | (2) |
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8-14 Effector T-cell functions are mediated by cytokines and cytotoxins |
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220 | (1) |
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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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221 | (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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222 | (1) |
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8-17 Cytotoxic T cells kill their target cells by inducing apoptosis |
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223 | (1) |
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8-18 Effector TH1 CD4 cells induce macrophage activation |
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224 | (1) |
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8-19 TFH cells, and the naive B cells that they help, recognize different epitopes of the same antigen |
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225 | (1) |
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8-20 Regulatory CD4 T cells limit the activities of effector CD4 and CD8 T cells |
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226 | (5) |
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227 | (1) |
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227 | (1) |
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228 | (3) |
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Chapter 9 Immunity Mediated by B Cells and Antibodies |
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231 | (36) |
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Antibody production by B lymphocytes |
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231 | (1) |
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9-1 B-cell activation requires cross-linking of surface immunoglobulin |
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232 | (1) |
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9-2 B-cell activation requires signals from the B-cell co-receptor |
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232 | (2) |
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9-3 Effective B cell-mediated immunity depends on help from CD4 T cells |
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234 | (1) |
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9-4 Follicular dendritic cells in the B-cell area store and display intact antigens to B cells |
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235 | (1) |
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9-5 Antigen-activated B cells move close to the T-cell area to find a helper TFH cell |
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236 | (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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238 | (1) |
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9-7 Activated B cells undergo somatic hypermutation and isotype switching in the specialized microenvironment of the primary follicle |
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239 | (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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241 | (2) |
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9-9 The cytokines made by helper T cells determine how B cells switch their immunoglobulin isotype |
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243 | (1) |
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9-10 Cytokines made by helper T cells determine the differentiation of antigen-activated B cells into plasma cells or memory cells |
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244 | (2) |
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245 | (1) |
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Antibody effector functions |
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245 | (1) |
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9-11 IgM, IgG, and monomeric IgA protect the internal tissues of the body |
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246 | (1) |
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9-12 Dimeric IgA protects the mucosal surfaces of the body |
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246 | (1) |
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9-13 IgE provides a mechanism for the rapid ejection of parasites and other pathogens from the body |
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247 | (3) |
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9-14 Mothers provide protective antibodies to their young, both before and after birth |
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250 | (1) |
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9-15 High-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells |
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251 | (2) |
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9-16 High-affinity IgG and IgA antibodies are used to neutralize microbial toxins and animal venoms |
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253 | (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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255 | (1) |
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9-18 Two forms of C4 tend to be fixed at different sites on pathogen surfaces |
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256 | (1) |
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9-19 Complement activation by IgG requires the participation of two or more IgG molecules |
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257 | (1) |
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9-20 Erythrocytes facilitate the removal of immune complexes from the circulation |
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258 | (1) |
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9-21 Fey receptors enable effector cells to bind and be activated by IgG bound to pathogens |
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258 | (2) |
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9-22 A variety of low-affinity Fc receptors are IgG-specific |
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260 | (1) |
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9-23 An Fc receptor acts as an antigen receptor for NK cells |
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261 | (1) |
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9-24 The Fc receptor for monomeric IgA belongs to a different family than the Fc receptors for IgG and IgE |
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262 | (5) |
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263 | (1) |
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263 | (1) |
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264 | (3) |
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Chapter 10 Preventing Infection at Mucosal Surfaces |
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267 | (28) |
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10-1 The communication functions of mucosal surfaces render them vulnerable to infection |
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267 | (2) |
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10-2 Mucins are gigantic glycoproteins that endow the mucus with the properties to protect epithelial surfaces |
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269 | (1) |
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10-3 Commensal microorganisms assist the gut in digesting food and maintaining health |
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269 | (3) |
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10-4 The gastrointestinal tract is invested with distinctive secondary lymphoid tissues |
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272 | (1) |
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10-5 Inflammation of mucosal tissues is associated with causation not cure of disease |
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273 | (2) |
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10-6 Intestinal epithelial cells contribute to innate immune responses in the gut |
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275 | (1) |
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10-7 Intestinal macrophages eliminate pathogens without creating a state of inflammation |
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276 | (1) |
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10-8 M cells constantly transport microbes and antigens from the gut lumen to gut-associated lymphoid tissue |
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277 | (1) |
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10-9 Gut dendritic cells respond differently to food, commensal microorganisms, and pathogens |
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278 | (1) |
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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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279 | (2) |
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10-11 A variety of effector lymphocytes guard healthy mucosal tissue in the absence of infection |
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281 | (1) |
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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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282 | (1) |
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10-13 Secretory IgM and IgA protect mucosal surfaces from microbial invasion |
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283 | (2) |
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10-14 Two subclasses of IgA have complementary properties for controlling microbial populations |
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285 | (1) |
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10-15 People lacking IgA are able to survive, reproduce, and generally remain W healthy |
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286 | (2) |
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10-16 TH2-mediated immunity protects against helminth infections |
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288 | (7) |
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290 | (2) |
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292 | (3) |
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Chapter 11 Immunological Memory and Vaccination |
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295 | (34) |
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Immunological memory and the secondary immune response |
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296 | (1) |
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11-1 Antibodies made in a primary immune response persist for several months and provide protection |
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296 | (1) |
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11-2 Low levels of pathogen-specific antibodies are maintained by long-lived plasma cells |
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297 | (1) |
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11-3 Long-lived clones of memory B cells and T cells are produced in the primary immune response |
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297 | (2) |
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11-4 Memory B cells and T cells provide protection against pathogens for decades and even for life |
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299 | (1) |
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11-5 Maintaining populations of memory cells does not depend upon the persistence of antigen |
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299 | (1) |
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11-6 Changes to the antigen receptor distinguish naive, effector, and memory B cells |
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300 | (1) |
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11-7 In the secondary immune response, memory B cells are activated whereas naive B cells are inhibited |
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300 | (1) |
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11-8 Activation of the primary and secondary immune responses have common features |
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301 | (1) |
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11-9 Combinations of cell-surface markers distinguish memory T cells from naive and effector T cells |
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302 | (2) |
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11-10 Central and effector memory T cells recognize pathogens in different tissues of the body |
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304 | (1) |
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11-11 In viral infections, numerous effector CD8 T cells give rise to relatively few memory T cells |
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305 | (1) |
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11-12 Immune-complex-mediated inhibition of naive B cells is used to prevent hemolytic anemia of the newborn |
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305 | (1) |
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11-13 In the response to influenza virus, immunological memory is gradually eroded |
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306 | (2) |
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307 | (1) |
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Vaccination to prevent infectious disease |
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308 | (1) |
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11-14 Protection against smallpox is achieved by immunization with the less dangerous cowpox virus |
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308 | (1) |
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11-15 Smallpox is the only infectious disease of humans that has been eradicated worldwide by vaccination |
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309 | (1) |
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11-16 Most viral vaccines are made from killed or inactivated viruses |
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310 | (1) |
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11-17 Both inactivated and live-attenuated vaccines protect against poliovirus |
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311 | (1) |
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11-18 Vaccination can inadvertently cause disease |
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312 | (1) |
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11-19 Subunit vaccines are made from the most antigenic components of a pathogen |
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313 | (1) |
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11-20 Invention of rotavirus vaccines took at least 30 years of research and development |
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313 | (1) |
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11-21 Bacterial vaccines are made from whole bacteria, secreted toxins, or capsular polysaccharides |
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314 | (1) |
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11-22 Conjugate vaccines enable high-affinity antibodies to be made against carbohydrate antigens |
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315 | (1) |
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11-23 Adjuvants are added to vaccines to activate and enhance the response to antigen |
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316 | (1) |
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11-24 Genome sequences of human pathogens have opened up new avenues for making vaccines |
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316 | (2) |
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11-25 The ever-changing influenza virus requires a new vaccine every year |
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318 | (1) |
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11-26 The need for a vaccine and the demands placed upon it change with the prevalence of disease |
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319 | (3) |
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11-27 Vaccines have yet to be made against pathogens that establish chronic infections |
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322 | (1) |
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11-28 Vaccine development faces greater public scrutiny than drug development |
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323 | (6) |
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324 | (1) |
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325 | (1) |
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326 | (3) |
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Chapter 12 Coevolution of Innate and Adaptive Immunity |
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329 | (36) |
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Regulation of NK-cell function by MHC class I and related molecules |
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330 | (1) |
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12-1 NK cells express a range of activating and inhibitory receptors |
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330 | (2) |
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12-2 The strongest receptor that activates NK cells is an Fc receptor |
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332 | (1) |
|
12-3 Many NK-cell receptors recognize MHC class I and related molecules |
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333 | (2) |
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12-4 Immunoglobulin-like NK-cell receptors recognize polymorphic epitopes of HLA-A, HLA-B, and HLA-C |
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335 | (1) |
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12-5 NK cells are educated to detect pathological change in MHC class I Expression |
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336 | (3) |
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12-6 Different genomic complexes encode lectin-like and immunoglobulin-like NK-cell receptors |
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339 | (1) |
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12-7 Human KIR haplotypes uniquely come in two distinctive forms |
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340 | (1) |
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12-8 Cytomegalovirus infection induces proliferation of NK cells expressing the activating HLA-E receptor |
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341 | (1) |
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12-9 Interactions of uterine NK cells with fetal MHC class I molecules affect reproductive success |
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342 | (5) |
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345 | (2) |
|
Maintenance of tissue integrity by γ:δ cells |
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347 | (1) |
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12-10 γ:δ T cells are not governed by the same rules as α:β T cells |
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347 | (1) |
|
12-11 γ:δ T cells in blood and tissues express different γ:δ receptors |
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348 | (2) |
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12-12 Vγ9: Vγ2 T cells recognize phosphoantigens presented on cell surfaces |
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350 | (1) |
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12-13 Vγ4: Vγ5 T cells detect both virus-infected cells and tumor cells |
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351 | (1) |
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12-14 Vγ: Vγ1 T-cell receptors recognize lipid antigens presented by CD1d |
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352 | (2) |
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354 | (1) |
|
Restriction of α:β T cells by non-polymorphic MHC class l-like molecules |
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354 | (1) |
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12-15 CD1-restricted α:β T cells recognize lipid antigens of mycobacterial pathogens |
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354 | (2) |
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12-16 NKT cells are innate lymphocytes that detect lipid antigens by using α:β T-cell receptors |
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356 | (1) |
|
12-17 Mucosa-associated invariant T cells detect bacteria and fungi that make riboflavin |
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357 | (8) |
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359 | (1) |
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360 | (1) |
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361 | (4) |
|
Chapter 13 Failures of the Body's Defenses |
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365 | (36) |
|
Evasion and subversion of the immune system by pathogens |
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|
365 | (1) |
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13-1 Genetic variation within some species of pathogens prevents effective long-term immunity |
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366 | (1) |
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13-2 Mutation and recombination allow influenza virus to escape from immunity |
|
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366 | (2) |
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13-3 Trypanosomes use gene conversion to change their surface antigens |
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368 | (1) |
|
13-4 Herpesviruses persist in human hosts by hiding from the immune response |
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369 | (2) |
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13-5 Some pathogens sabotage or subvert immune defense mechanisms |
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371 | (2) |
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13-6 Bacterial superantigens stimulate a massive but ineffective CD4 T-cell response |
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373 | (1) |
|
13-7 Subversion of IgA action by bacterial IgA-binding proteins |
|
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374 | (1) |
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375 | (1) |
|
Inherited immunodeficiency diseases |
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375 | (1) |
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13-8 Rare primary immunodeficiency diseases reveal how the human immune system works |
|
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375 | (2) |
|
13-9 Inherited immunodeficiency diseases are caused by dominant, recessive, or X-linked gene defects |
|
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377 | (1) |
|
13-10 Recessive and dominant mutations in the IFN-γ receptor cause diseases of differing severity |
|
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378 | (1) |
|
13-11 Antibody deficiency leads to poor clearing of extracellular bacteria |
|
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379 | (1) |
|
13-12 Diminished production of antibodies M also results from inherited defects in T-cell help |
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380 | (1) |
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13-13 Complement defects impair antibody-mediated immunity and cause immune-complex disease |
|
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381 | (1) |
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13-14 Defects in phagocytes result in enhanced susceptibility to bacterial infection |
|
|
382 | (1) |
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13-15 Defects in T-cell function result in severe combined immune deficiencies |
|
|
383 | (2) |
|
13-16 Some inherited immunodeficiencies lead to specific disease susceptibilities |
|
|
385 | (3) |
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|
|
386 | (1) |
|
Acquired immune deficiency syndrome |
|
|
386 | (2) |
|
13-17 HIV is a retrovirus that causes a slowly progressing chronic disease |
|
|
388 | (1) |
|
13-18 HIV infects CD4T cells, macrophages, and dendritic cells |
|
|
388 | (1) |
|
13-19 In the twentieth century, most HIV-infected people progressed in time to get AIDS |
|
|
389 | (2) |
|
13-20 Genetic deficiency of the CCR5 co-receptor for HIV confers resistance to infection |
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|
391 | (1) |
|
13-21 HLA and KIR polymorphisms influence the progression to AIDS |
|
|
392 | (1) |
|
13-22 HIV escapes the immune response and develops resistance to antiviral drugs by rapid mutation |
|
|
393 | (1) |
|
13-23 Clinical latency is a period of active infection and renewal of CD4 T cells |
|
|
394 | (1) |
|
13-24 HIV infection leads to immunodeficiency and death from opportunistic infections |
|
|
395 | (1) |
|
13-25 A minority of HIV-infected individuals make antibodies that neutralize many strains of HIV |
|
|
396 | (5) |
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|
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397 | (1) |
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|
398 | (1) |
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|
398 | (3) |
|
Chapter 14 IgE-Mediated Immunity and Allergy |
|
|
401 | (32) |
|
14-1 Different effector mechanisms cause four distinctive types of hypersensitivity reaction |
|
|
401 | (3) |
|
Shared mechanisms of immunity and allergy |
|
|
403 | (1) |
|
14-2 IgE-mediated immune responses defend the body against multicellular parasites |
|
|
404 | (1) |
|
14-3 IgE antibodies emerge at early and late times in the primary immune response |
|
|
404 | (2) |
|
14-4 Allergy is prevalent in countries where parasite infections have been eliminated |
|
|
406 | (1) |
|
14-5 IgE has distinctive properties that contrast with those of IgG |
|
|
406 | (1) |
|
14-6 IgE and FceRI supply each mast cell with a diversity of antigen-specific receptors |
|
|
407 | (1) |
|
14-7 FceRII is a low-affinity receptor for IgE Fc regions that regulates the production of IgE by B cells |
|
|
407 | (2) |
|
14-8 Treatment of allergic disease with an IgE-specific monoclonal antibody |
|
|
409 | (1) |
|
14-9 Mast cells defend and maintain the tissues in which they reside |
|
|
410 | (1) |
|
14-10 Tissue mast cells orchestrate IgE-mediated reactions through the release of inflammatory mediators |
|
|
411 | (2) |
|
14-11 Eosinophils are specialized granulocytes that release toxic mediators in IgE-mediated responses |
|
|
413 | (2) |
|
14-12 Basophils are rare granulocytes that initiate TH2 responses and the production of IgE |
|
|
415 | (1) |
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|
|
415 | (1) |
|
IgE-mediated allergic disease |
|
|
416 | (1) |
|
14-13 Allergens are protein antigens, some of which resemble parasite antigens |
|
|
416 | (2) |
|
14-14 Predisposition to allergic disease is influenced by genetic and environmental factors |
|
|
418 | (1) |
|
14-15 IgE-mediated allergic reactions consist of an immediate response followed by a late-phase response |
|
|
419 | (1) |
|
14-16 The effects of IgE-mediated allergic reactions vary with the site of mast-cell activation |
|
|
420 | (1) |
|
14-17 Systemic anaphylaxis is caused by allergens in the blood |
|
|
421 | (2) |
|
14-18 Rhinitis and asthma are caused by inhaled allergens |
|
|
423 | (1) |
|
14-19 Urticaria, angioedema, and eczema are allergic reactions in the skin |
|
|
424 | (2) |
|
14-20 Food allergies cause systemic effects as well as gut reactions |
|
|
426 | (1) |
|
14-21 Allergic reactions are prevented and treated by three complementary approaches |
|
|
427 | (6) |
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|
|
428 | (1) |
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|
|
428 | (1) |
|
|
|
429 | (4) |
|
Chapter 15 Transplantation of Tissues and Organs |
|
|
433 | (40) |
|
Allogeneic transplantation can trigger hypersensitivity reactions |
|
|
433 | (1) |
|
15-1 Blood is the most common transplanted tissue |
|
|
434 | (1) |
|
15-2 Before blood transfusion, donors and recipients are matched for ABO and the Rhesus D antigens |
|
|
434 | (1) |
|
15-3 Incompatibility of blood group antigens causes type II hypersensitivity reactions |
|
|
435 | (1) |
|
15-4 Hyperacute rejection of transplanted organs is a type II hypersensitivity reaction |
|
|
436 | (1) |
|
15-5 Anti-HLA antibodies can arise from pregnancy, blood transfusion, or previous transplants |
|
|
437 | (1) |
|
15-6 Transplant rejection and graft-versus-host disease are type IV hypersensitivity reactions |
|
|
438 | (2) |
|
|
|
439 | (1) |
|
Transplantation of solid organs |
|
|
440 | (1) |
|
15-7 Organ transplantation involves procedures that inflame the donated organ and the transplant recipient |
|
|
440 | (1) |
|
15-8 Acute rejection is a type IV hypersensitivity caused by effector T cells responding to HLA differences between donor and recipient |
|
|
441 | (1) |
|
15-9 HLA differences between transplant donor and recipient activate numerous alloreactive T cells |
|
|
442 | (1) |
|
15-10 Chronic rejection of organ transplants is caused by a type III hypersensitivity reaction |
|
|
443 | (2) |
|
15-11 Matching donor and recipient HLA class I and II allotypes improves the success of transplantation |
|
|
445 | (1) |
|
15-12 Immunosuppressive drugs make allogeneic transplantation possible as routine therapy |
|
|
445 | (2) |
|
15-13 Some treatments induce immunosuppression before transplantation |
|
|
447 | (1) |
|
15-14 T-cell activation can be targeted by immunosuppressive drugs |
|
|
448 | (3) |
|
15-15 Alloreactive T-cell co-stimulation can be blocked with a soluble form of CTLA4 |
|
|
451 | (1) |
|
15-16 Blocking cytokine signaling can prevent alloreactive T-cell activation |
|
|
452 | (1) |
|
15-17 Cytotoxic drugs target the replication and proliferation of alloantigen-activated T cells |
|
|
453 | (2) |
|
15-18 Patients needing a transplant outnumber the available organs |
|
|
455 | (1) |
|
15-19 The need for HLA matching and immunosuppressive therapy varies with the organ transplanted |
|
|
456 | (3) |
|
|
|
457 | (1) |
|
Hematopoietic cell transplantation |
|
|
458 | (1) |
|
15-20 Hematopoietic cell transplantation is a treatment for genetic diseases of blood cells |
|
|
459 | (2) |
|
15-21 Allogeneic hematopoietic cell transplantation is the preferred treatment for many cancers |
|
|
461 | (1) |
|
15-22 After hematopoietic cell transplantation, the patient is attacked by alloreactive T cells in the graft |
|
|
461 | (1) |
|
15-23 HLA matching of donor and recipient is most important for hematopoietic cell transplantation |
|
|
462 | (2) |
|
15-24 Minor histocompatibility antigens trigger alloreactive T cells in recipients of HLA-identical transplants |
|
|
464 | (1) |
|
15-25 Some GVHD helps engraftment and prevents relapse of malignant disease |
|
|
465 | (1) |
|
15-26 NK cells also mediate graft-versus-leukemia effects |
|
|
466 | (1) |
|
15-27 Hematopoietic cell transplantation can induce tolerance of a solid organ transplant |
|
|
467 | (6) |
|
|
|
467 | (1) |
|
|
|
468 | (1) |
|
|
|
469 | (4) |
|
Chapter 16 Disruption of Healthy Tissue by the Adaptive Immune Response |
|
|
473 | (36) |
|
16-1 Every autoimmune disease resembles a type II, III, or IV hypersensitivity reaction |
|
|
474 | (3) |
|
16-2 Autoimmune diseases arise when tolerance to self antigens is lost |
|
|
477 | (1) |
|
16-3 HLA is the dominant genetic factor affecting susceptibility to autoimmune disease |
|
|
478 | (2) |
|
16-4 HLA associations reflect the importance of T-cell tolerance in preventing autoimmunity |
|
|
480 | (1) |
|
16-5 Binding of antibodies to cell-surface receptors causes several autoimmune diseases |
|
|
481 | (3) |
|
16-6 Organized lymphoid tissue sometimes forms at sites inflamed by autoimmune disease |
|
|
484 | (1) |
|
16-7 The antibody response to an autoantigen can broaden and strengthen by epitope spreading |
|
|
485 | (2) |
|
16-8 Intermolecular epitope spreading occurs in systemic autoimmune disease |
|
|
487 | (2) |
|
16-9 Intravenous immunoglobulin is a therapy for autoimmune diseases |
|
|
489 | (1) |
|
16-10 Monoclonal antibodies that target TNF-α and B cells are used to treat rheumatoid arthritis |
|
|
490 | (1) |
|
16-11 Rheumatoid arthritis is influenced by genetic and environmental factors |
|
|
491 | (1) |
|
16-12 Autoimmune disease can be an adverse side-effect of an immune response to infection |
|
|
492 | (2) |
|
16-13 Noninfectious environmental factors affect the development of autoimmune disease |
|
|
494 | (1) |
|
16-14 Type 1 diabetes is caused by the selective destruction of insulin-producing cells in the pancreas |
|
|
495 | (1) |
|
16-15 Combinations of HLA class II allotypes confer susceptibility and resistance to type 1 diabetes |
|
|
496 | (2) |
|
16-16 Celiac disease is a hypersensitivity to food that has much in common with autoimmune disease |
|
|
498 | (1) |
|
16-17 Celiac disease is caused by the selective destruction of intestinal epithelial cells |
|
|
498 | (3) |
|
16-18 Senescence of the thymus and the T-cell population contributes to autoimmunity |
|
|
501 | (1) |
|
16-19 Autoinflammatory diseases of innate immunity |
|
|
502 | (7) |
|
|
|
503 | (3) |
|
|
|
506 | (3) |
|
Chapter 17 Cancer and Its Interactions With the Immune System |
|
|
509 | |
|
17-1 Cancer results from mutations that cause uncontrolled cell growth |
|
|
510 | (1) |
|
17-2 A cancer arises from a single cell that has accumulated multiple mutations |
|
|
510 | (2) |
|
17-3 Exposure to chemicals, radiation, and viruses facilitates progression to cancer |
|
|
512 | (1) |
|
17-4 Certain common features distinguish cancer cells from normal cells |
|
|
513 | (1) |
|
17-5 Immune responses to cancer have similarities with those to virus-infected cells |
|
|
514 | (1) |
|
17-6 Allogeneic differences in MHC class I molecules enable cytotoxic T cells to eliminate tumor cells |
|
|
515 | (1) |
|
17-7 Mutations acquired by somatic cells during oncogenesis can give rise to tumor-specific antigens |
|
|
516 | (1) |
|
17-8 Cancer/testis antigens are a prominent type of tumor-associated antigen |
|
|
517 | (1) |
|
17-9 Successful tumors evade and manipulate the immune response |
|
|
518 | (1) |
|
17-10 Vaccination against human papillomaviruses can prevent cervical and other genital cancers |
|
|
519 | (1) |
|
17-11 Vaccination with tumor antigens can cause cancer to regress but it is unpredictable |
|
|
520 | (1) |
|
17-12 Monoclonal antibodies that interfere with negative regulators of the immune response can be used to treat cancer |
|
|
521 | (1) |
|
17-13 T-cell responses to tumor cells can be improved with chimeric antigen receptors |
|
|
522 | (2) |
|
17-14 The antitumor response of γ:δ T cells and NK cells can be augmented |
|
|
524 | (1) |
|
17-15 T-cell responses to tumors can be improved by adoptive transfer of antigen-activated dendritic cells |
|
|
525 | (1) |
|
17-16 Monoclonal antibodies are valuable tools for the diagnosis of cancer |
|
|
526 | (2) |
|
17-17 Monoclonal antibodies against cell-surface antigens are increasingly used in cancer therapy |
|
|
528 | |
|
|
|
529 | (1) |
|
|
|
530 | |
