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Elements of the Immune System and their Roles in Defense |
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1 | (36) |
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Defenses facing invading pathogens |
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2 | (1) |
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Pathogens are infectious organisms that cause disease |
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2 | (3) |
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The skin and mucosal surfaces form physical barriers against infection |
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5 | (2) |
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The innate immune response causes inflammation at sites of infection |
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7 | (1) |
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The adaptive immune response adds to an ongoing innate immune response |
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8 | (3) |
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Immune system cells with different functions all derive from hematopoietic stem cells |
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11 | (4) |
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Most lymphocytes are present in specialized lymphoid tissues |
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15 | (1) |
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Lymphocytes are activated in the secondary lymphoid tissues |
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16 | (5) |
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20 | (1) |
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Principles of adaptive immunity |
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20 | (1) |
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Immunoglobulins and T-cell receptors are the highly variable recognition molecules of adaptive immunity |
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21 | (1) |
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The diversity of immunoglobulins and T-cell receptors is generated by gene rearrangement |
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22 | (1) |
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B cells recognize intact pathogens, whereas T cells recognize pathogen-derived peptides bound to proteins of the major histocompatibility complex |
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23 | (1) |
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Clonal selection of B and T lymphocytes is the guiding principle of the adaptive immune response |
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24 | (2) |
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Extracellular pathogens and their toxins are eliminated by antibodies |
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26 | (2) |
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Adaptive immune responses generally give rise to long-lived immunological memory and protective immunity |
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28 | (1) |
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The immune system can be compromised by inherited immunodeficiencies or by the actions of certain pathogens |
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29 | (1) |
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Unwanted effects of adaptive immunity cause allergy, autoimmune disease, and rejection of transplanted tissues |
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30 | (7) |
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32 | (1) |
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33 | (1) |
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34 | (3) |
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Antibody Structure and the Generation of B-Cell Diversity |
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37 | (30) |
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The structural basis of antibody diversity |
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38 | (1) |
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Antibodies are composed of polypeptides with variable and constant regions |
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38 | (2) |
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Immunoglobulin chains are folded into compact and stable protein domains |
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40 | (1) |
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An antigen-binding site is formed from the hypervariable regions of a heavy-chain and a light-chain V domain |
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41 | (1) |
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Antigen-binding sites vary in shape and physical properties |
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42 | (3) |
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Monoclonal antibodies are produced from a clone of antibody-producing cells |
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45 | (3) |
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47 | (1) |
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Generation of immunoglobulin diversity in B cells before encounter with antigen |
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47 | (1) |
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The DNA sequence encoding a V region is assembled from two or three gene segments |
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48 | (1) |
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Random recombination of gene segments produces diversity in the antigen-binding sites of immunoglobulins |
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49 | (2) |
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Recombination enzymes produce additional diversity in the antigen-binding sites of immunoglobulins |
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51 | (1) |
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Naive B cells use alternative mRNA splicing to make both IgM and IgD |
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52 | (1) |
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Each B cell produces immunoglobulin of a single antigen specificity |
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52 | (2) |
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Immunoglobulin is first made in a membrane-bound form that is present on the B-cell surface |
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54 | (1) |
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54 | (1) |
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Diversification of antibodies after B cells encounter antigen |
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55 | (1) |
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Secreted antibodies are produced by an alternative pattern of heavy-chain RNA processing |
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55 | (1) |
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Rearranged V-region sequences are further diversified by somatic hypermutation |
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56 | (1) |
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Isotype switching produces immunoglobulins with different C regions but identical antigen specificities |
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57 | (1) |
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Antibodies with different C regions have different effector functions |
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58 | (9) |
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61 | (1) |
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61 | (2) |
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63 | (4) |
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Antigen Recognition by T Lymphocytes |
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67 | (32) |
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T-cell receptor diversity |
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68 | (1) |
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The T-cell receptor resembles a membrane-associated Fab fragment of immunoglobulin |
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68 | (1) |
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T-cell receptor diversity is generated by gene rearrangement |
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69 | (2) |
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Expression of the T-cell receptor on the cell surface requires association with additional proteins |
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71 | (1) |
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γ and δ chains form a second class of T-cell receptor expressed by a distinct population of T cells |
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71 | (3) |
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73 | (1) |
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Antigen processing and presentation |
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73 | (1) |
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Two classes of T cell are specialized to respond to intracellular and extracellular sources of infection |
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74 | (1) |
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Two classes of MHC molecule present antigen to CD8 and CD4 T cells respectively |
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75 | (1) |
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The two classes of MHC molecule have similar three-dimensional structures |
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76 | (1) |
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MHC molecules bind a variety of peptides |
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77 | (1) |
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Peptides generated in the cytosol are transported into the endoplasmic reticulum where they bind MHC class I molecules |
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78 | (2) |
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Peptides presented by MHC class II molecules are generated in acidified intracellular vesicles |
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80 | (2) |
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MHC class II molecules are prevented from binding peptides in the endoplasmic reticulum by the invariant chain |
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82 | (1) |
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The T-cell receptor specifically recognizes both peptide and MHC molecule |
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83 | (1) |
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The two classes of MHC molecule are expressed differentially on cells |
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83 | (3) |
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85 | (1) |
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The major histocompatibility complex |
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86 | (1) |
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The diversity of MHC molecules in the human population is due to multigene families and genetic polymorphism |
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86 | (1) |
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The MHC class I and class II genes occupy different regions of the MHC |
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87 | (1) |
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Other proteins involved in antigen processing and presentation are encoded in the MHC class II region |
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88 | (1) |
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MHC polymorphism affects the binding and presentation of peptide antigens to T cells |
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89 | (1) |
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MHC diversity results from selection by infectious disease |
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90 | (3) |
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MHC polymorphism triggers T-cell reactions that can reject transplanted organs |
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93 | (6) |
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94 | (1) |
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95 | (1) |
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95 | (4) |
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The Development of B Lymphocytes |
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99 | (12) |
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The development of B cells in the bone marrow |
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99 | (1) |
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B-cell development in the bone marrow proceeds through several stages |
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100 | (2) |
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The survival of a developing B cell depends on the productive rearrangement of a heavy- and a light-chain gene |
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102 | (3) |
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Cell-surface expression of the products of rearranged immunoglobulin genes prevents further gene rearrangement |
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105 | (1) |
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The proteins involved in immunoglobulingene rearrangement are controlled developmentally |
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106 | (2) |
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Many B-cell tumors carry chromosomal translocations that join immunoglobulin genes to genes regulating cell growth |
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108 | (1) |
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B cells expressing the glycoprotein CD5 express a distinctive repertoire of receptors |
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108 | (3) |
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110 | (1) |
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Selection and further development of the B-cell repertoire |
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110 | (1) |
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Self-reactive immature B cells are altered, eliminated, or inactivated by contact with self-antigens |
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111 | (12) |
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Mature, naive B cells compete for access to lymphoid follicles |
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112 | (1) |
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Encounter with antigen leads to the differentiation of activated B cells into plasma cells and memory B cells |
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113 | (2) |
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Different types of B-cell tumor reflect B cells at different stages of development |
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115 | (8) |
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116 | (1) |
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117 | (2) |
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119 | (4) |
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The Development of T Lymphocytes |
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123 | (22) |
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The development of T cells in the thymus |
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124 | (1) |
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T cells develop in the thymus |
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124 | (1) |
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The two lineages of T cells arise from a common thymocyte progenitor |
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125 | (1) |
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Production of a T-cell receptor β chain leads to cessation of β-chain gene rearrangement and to expression of CD4 and CD8 |
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126 | (3) |
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T-cell receptor α-chain genes can undergo several successive rearrangements |
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129 | (2) |
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Cells expressing particular γ:δ receptors arise first in embryonic development |
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131 | (1) |
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131 | (1) |
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Positive and negative selection of the T-cell repertoire |
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131 | (1) |
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T cells that can recognize self-MHC molecules are positively selected in the thymus |
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132 | (1) |
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Positive selection controls expression of the CD4 or CD8 co-receptor |
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133 | (1) |
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Rearrangement of α-chain genes stops once a cell has been positively selected |
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134 | (1) |
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T cells specific for self-antigens are removed in the thymus by negative selection |
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135 | (1) |
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T cells undergo further differentiation in secondary lymphoid tissues after encounter with antigen |
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136 | (1) |
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The requirements of thymic selection can limit the number of functional class I and class II genes in the MHC |
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137 | (2) |
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Most T-cell tumors represent early or late stages of T-cell development |
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139 | (6) |
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139 | (1) |
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140 | (2) |
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142 | (3) |
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145 | (36) |
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Activation of naive T cells on encounter with antigen |
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145 | (1) |
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Dendritic cells carry antigens from sites of infection to secondary lymphoid tissues |
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146 | (1) |
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Naive T cells first encounter antigen on antigen-presenting cells in secondary lymphoid tissues |
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147 | (1) |
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Homing of naive T cells to secondary lymphoid tissues is determined by cell adhesion molecules |
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148 | (2) |
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Activation of naive T cells requires a co-stimulatory signal delivered by a professional antigen-presenting cell |
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150 | (1) |
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Secondary lymphoid tissues contain three kinds of professional antigen-presenting cell |
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151 | (4) |
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When T cells are activated by antigen, signals from T-cell receptors and co-receptors alter the pattern of gene transcription |
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155 | (3) |
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Proliferation and differentiation of activated T cells are driven by the cytokine interleukin-2 |
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158 | (1) |
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Antigen recognition by a naive T cell in the absence of co-stimulation leads to the T cell becoming nonresponsive |
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159 | (1) |
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On activation, CD4 T cells can acquire different helper functions |
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159 | (1) |
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Naive CD8 T cells can be activated in different ways to become cytotoxic effector cells |
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160 | (1) |
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161 | (2) |
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The properties and functions of effector T cells |
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163 | (1) |
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Effector T cells can be stimulated by antigen in the absence of co-stimulatory signals |
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163 | (1) |
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Effector T-cell functions are performed by cytokines and cytotoxins |
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164 | (1) |
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Cytotoxic CD8 T cells are selective and serial killers of target cells at sites of infection |
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165 | (3) |
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Cytotoxic T cells kill their target cells by inducing apoptosis |
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168 | (1) |
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TH1 CD4 cells induce macrophages to become activated |
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169 | (2) |
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TH1 cells coordinate the host response to intravesicular pathogens |
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171 | (1) |
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CD4 TH2 cells activate only those B cells that recognize the same antigen as they do |
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172 | (1) |
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Regulatory CD4 T cells limit the activities of effector CD4 and CD8 T cells |
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173 | (8) |
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174 | (1) |
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175 | (2) |
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177 | (4) |
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Immunity Mediated by B Cells and Antibodies |
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181 | (46) |
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Antibody production by B lymphocytes |
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182 | (1) |
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B-cell activation requires cross-linking of surface immunoglobulin |
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182 | (1) |
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The antibody response to certain antigens does not require T-cell help |
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183 | (2) |
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B cells needing T-cell help are activated in secondary lymphoid tissues where they form germinal centers |
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185 | (3) |
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Activated B cells undergo somatic hypermutation and affinity maturation in the specialized microenvironment of the germinal center |
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188 | (4) |
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Interactions with T cells are required for isotype switching in B cells |
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192 | (2) |
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193 | (1) |
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Antibody effector functions |
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194 | (1) |
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IgM, IgG, and IgA antibodies protect the blood and extracellular fluids |
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194 | (1) |
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IgA and IgG are transported across epithelial barriers by specific receptor proteins |
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195 | (2) |
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Antibody production is deficient in very young infants |
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197 | (1) |
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High-affinity IgG and IgA antibodies are used to neutralize microbial toxins and animal venoms |
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197 | (2) |
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High-affinity neutralizing antibodies prevent viruses and bacteria from infecting cells |
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199 | (1) |
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The Fc receptors of hematopoietic cells are signaling receptors that bind the Fc regions of antibodies |
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200 | (1) |
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Phagocyte Fc receptors facilitate the recognition, uptake, and destruction of antibody-coated pathogens |
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201 | (1) |
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IgE binds to high-affinity Fc receptors on mast cells, basophils, and activated eosinophils |
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202 | (2) |
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Fc receptors activate natural killer cells to destroy antibody-coated human cells |
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204 | (2) |
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205 | (1) |
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The antigen--antibody mediated pathway of complement activation |
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205 | (1) |
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Complement components are plasma proteins with various functions |
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206 | (1) |
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C1 uses different polypeptides to bind antibody and to activate complement components |
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207 | (2) |
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Fragments of C2 and C4 associate on the pathogen surface to form the classical C3 convertase |
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209 | (1) |
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Cleavage of C3 yields C3b covalently bound to pathogen surfaces |
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210 | (1) |
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Partial lack of C4 is the most common immune protein deficiency in humans |
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210 | (1) |
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C3b produced by the classical C3 convertase permits the formation of a more powerful alternative C3 convertase |
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211 | (1) |
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Fragments of C3 and C4 on pathogen surfaces are recognized by receptors on various cell types |
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212 | (2) |
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Complement receptors remove immune complexes from the circulation |
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214 | (1) |
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The terminal complement proteins lyse pathogens by forming a membrane pore |
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215 | (1) |
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Small peptides released during complement activation induce local inflammation |
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216 | (1) |
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Regulatory proteins in plasma limit the extent of complement activation |
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217 | (3) |
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Regulatory proteins on human cell surfaces protect them from the effects of complement activation |
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220 | (7) |
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221 | (1) |
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222 | (2) |
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224 | (3) |
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The Body's Defenses Against Infection |
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227 | (52) |
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227 | (1) |
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Infectious diseases are caused by pathogens of diverse types that live and replicate in the human body |
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228 | (4) |
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Surface epithelia present a formidable barrier to infection |
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232 | (1) |
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Complement activation by the alternative pathway tags microorganisms for destruction |
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233 | (3) |
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Several classes of plasma protein limit the spread of infection |
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236 | (1) |
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Phagocytosis by macrophages provides a first line of cellular defense against invading microorganisms |
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237 | (1) |
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Receptors that detect microbial products signal macrophage activation |
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238 | (1) |
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Activation of resident macrophages induces inflammation at sites of infection |
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239 | (4) |
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Neutrophils are dedicated phagocytes that are summoned to sites of infection |
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243 | (1) |
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The homing of neutrophils to infected tissues is induced by inflammatory mediators |
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244 | (2) |
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Neutrophils are potent killers of pathogens and are themselves programmed to die |
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246 | (1) |
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Inflammatory cytokines raise body temperature and activate hepatocytes to make the acute-phase response |
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247 | (3) |
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Type I interferons inhibit viral replication and activate host defenses |
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250 | (2) |
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NK cells provide an early defense against intracellular infections |
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252 | (1) |
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NK-cell receptors differ in the ligands they bind and the signals they generate |
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253 | (2) |
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Three genetic complexes contribute to NK-cell recognition of `missing-self' |
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255 | (3) |
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Minority subpopulations of B and T cells contribute to innate immunity |
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258 | (2) |
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259 | (1) |
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Adaptive immune responses to infection |
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260 | (1) |
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Adaptive immune responses start with T-cell activation in secondary lymphoid tissues |
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260 | (2) |
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Microfold cells in the gut deliver antigens to Peyer's patches |
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262 | (1) |
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Primary CD4 T-cell responses are influenced by the cytokines made by cells of innate immunity |
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263 | (1) |
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Effector T cells are guided to sites of infection by newly expressed cell adhesion molecules |
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264 | (1) |
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Antibody responses develop in lymphoid tissues under the direction of TH2 cells |
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265 | (2) |
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Antibody secretion by plasma cells occurs at sites distinct from those at which B cells are activated by TH2 cells |
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267 | (2) |
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268 | (1) |
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Immunological memory and the secondary immune response |
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268 | (1) |
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Immunological memory after infection is long lived |
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269 | (1) |
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Pathogen-specific memory B cells are more abundant and make better antibodies than naive B cells |
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269 | (1) |
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T-cell memory is maintained by T cells that have different cell-surface markers from naive T cells |
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270 | (2) |
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Maintenance of immunological memory does not require stimulation with antigen |
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272 | (1) |
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The second and subsequent responses to a pathogen are mediated solely by memory lymphocytes and not by naive lymphocytes |
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273 | (6) |
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275 | (1) |
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275 | (1) |
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276 | (3) |
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Failures of the Body's Defenses |
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279 | (32) |
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Evasion and subversion of the immune system by pathogens |
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279 | (1) |
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Genetic variation within some species of pathogen prevents effective long-term immunity |
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280 | (1) |
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Mutation and recombination allow influenza virus to escape from immunity |
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280 | (1) |
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Trypanosomes use gene rearrangement to change their surface antigens |
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281 | (2) |
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Herpes viruses persist in human hosts by hiding from the immune response |
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283 | (1) |
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Certain pathogens sabotage or subvert immune defense mechanisms |
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284 | (2) |
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Bacterial superantigens stimulate a massive but ineffective T-cell response |
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286 | (1) |
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Immune responses can contribute to disease |
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286 | (1) |
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287 | (1) |
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Inherited immunodeficiency diseases |
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287 | (1) |
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Most inherited immunodeficiency diseases are caused by recessive gene defects |
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287 | (2) |
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Antibody deficiency leads to an inability to clear extracellular bacteria |
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289 | (2) |
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Diminished antibody production also results from inherited defects in T-cell help |
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291 | (1) |
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Defects in complement components impair antibody responses and cause the accumulation of immune complexes |
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291 | (1) |
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Defects in phagocytes result in enhanced susceptibility to bacterial infection |
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292 | (2) |
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Defects in T-cell function result in severe combined immune deficiencies |
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294 | (1) |
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Some inherited immunodeficiencies lead to specific disease susceptibilities |
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295 | (1) |
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Hematopoietic stem cell transplantation is used to correct genetic defects of the immune system |
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295 | (2) |
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296 | (1) |
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Acquired immune deficiency syndrome |
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296 | (1) |
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HIV is a retrovirus that causes slowly progressing disease |
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297 | (1) |
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HIV infects CD4 T cells, macrophages, and dendritic cells |
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298 | (1) |
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Most people who become infected with HIV progress in time to develop AIDS |
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299 | (3) |
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Genetic deficiency of the CCR5 co-receptor for HIV confers resistance to infection |
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302 | (1) |
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HIV escapes the immune response and develops resistance to antiviral drugs by rapid mutation |
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302 | (2) |
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Clinical latency is a period of active infection and renewal of CD4 T cells |
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304 | (1) |
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HIV infection leads to immunodeficiency and death from opportunistic infections |
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305 | (6) |
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306 | (1) |
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306 | (1) |
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307 | (4) |
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Over-reactions of the Immune System |
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311 | (32) |
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Four types of hypersensitivity reaction are caused by different effector mechanisms of adaptive immunity |
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311 | (2) |
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Type I hypersensitivity reactions |
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313 | (1) |
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IgE binds irreversibly to Fc receptors on mast cells, basophils, and activated eosinophils |
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313 | (1) |
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Tissue mast cells orchestrate IgE-mediated allergic reactions through the release of inflammatory mediators |
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314 | (3) |
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Eosinophils and basophils are specialized granulocytes that release toxic mediators in IgE-mediated responses |
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317 | (2) |
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Mast cells, basophils, and eosinophils can amplify an IgE response started by TH2 cells |
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319 | (1) |
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Common allergens are small proteins inhaled in particulate form that stimulate an IgE response |
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320 | (1) |
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Predisposition to allergy has a genetic basis |
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321 | (1) |
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IgE-mediated allergic reactions consist of an immediate response followed by a late-phase response |
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322 | (1) |
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The effects of IgE-mediated allergic reactions vary with the site of mast-cell activation |
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323 | (1) |
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Systemic anaphylaxis is caused by allergens in the blood |
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324 | (1) |
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Rhinitis and asthma are caused by inhaled allergens |
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325 | (1) |
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Urticaria, angioedema, and eczema are allergic reactions in the skin |
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326 | (2) |
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Food allergies cause systemic effects as well as gut reactions |
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328 | (1) |
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People with parasite infections and high levels of IgE rarely develop allergic disease |
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328 | (1) |
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Allergic reactions are prevented and treated by three complementary approaches |
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329 | (2) |
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330 | (1) |
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Type II, III, and IV hypersensitivity reactions |
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331 | (1) |
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Type II hypersensitivity reactions are caused by antibodies specific for altered components of human cells |
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331 | (2) |
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Type III hypersensitivity reactions are caused by immune complexes formed from IgG and soluble antigens |
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333 | (1) |
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Systemic disease caused by immune complexes can follow the administration of large quantities of soluble antigens |
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334 | (2) |
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Type IV hypersensitivity reactions are mediated by antigen-specific effector T cells |
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336 | (7) |
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338 | (1) |
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339 | (1) |
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339 | (4) |
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Disruption of Healthy Tissue by the Immune Response |
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343 | (36) |
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343 | (1) |
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The effector mechanisms of autoimmunity resemble those causing certain hypersensitivity reactions |
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344 | (2) |
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Endocrine glands contain specialized cells that are targets for organ-specific autoimmunity |
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346 | (1) |
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Autoimmune diseases of the thyroid can cause either underproduction or overproduction of thyroid hormones |
|
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347 | (1) |
|
The cause of autoimmune disease can be revealed by the transfer of disease with immune effectors |
|
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348 | (2) |
|
Insulin-dependent diabetes mellitus is caused by the selective destruction of insulin-producing cells in the pancreas |
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350 | (1) |
|
Autoantibodies against common components of human cells can cause systemic autoimmune disease |
|
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351 | (1) |
|
Most rheumatological diseases are caused by autoimmunity |
|
|
352 | (1) |
|
Multiple sclerosis and myasthenia gravis are autoimmune diseases of the nervous system |
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352 | (3) |
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|
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354 | (1) |
|
Genetic and environmental factors that predispose to autoimmune disease |
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355 | (1) |
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All autoimmune diseases involve breaking T-cell tolerance |
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355 | (1) |
|
Incomplete deletion of self-reactive T cells in the thymus causes autoimmune disease |
|
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356 | (1) |
|
Insufficient control of T-cell co-stimulation favors autoimmunity |
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357 | (1) |
|
Regulatory T cells protect cells and tissues from autoimmunity |
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358 | (1) |
|
HLA is the dominant genetic factor affecting susceptibility to autoimmune disease |
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359 | (2) |
|
Different combinations of HLA class II allotypes confer susceptibility and resistance to diabetes |
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361 | (1) |
|
Autoimmunity can be initiated by disease-associated HLA allotypes presenting antigens to autoimmune T cells |
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362 | (1) |
|
Noninfectious environmental factors influence the course of autoimmune diseases |
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363 | (1) |
|
Loss of oral tolerance leads to inflammation and autoimmunity |
|
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364 | (2) |
|
Infections are environmental factors that can trigger autoimmune disease |
|
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366 | (2) |
|
Autoimmune T cells can be activated in a pathogen-specific or nonspecific manner by infection |
|
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368 | (2) |
|
In the course of autoimmune disease the specificity of the autoimmune response broadens |
|
|
370 | (3) |
|
Senescence of the T-cell population can contribute to autoimmunity |
|
|
373 | (1) |
|
Do the current increases in hypersensitivity and autoimmune disease have a common cause? |
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373 | (6) |
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374 | (1) |
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|
374 | (1) |
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375 | (4) |
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Manipulation of the Immune Response |
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379 | (51) |
|
Prevention of infectious disease by vaccination |
|
|
379 | (1) |
|
Viral vaccines are made from whole viruses or viral components |
|
|
380 | (1) |
|
Bacterial vaccines are made from whole bacteria, their secreted toxins, or capsular polysaccharides |
|
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381 | (2) |
|
Adjuvants nonspecifically enhance the immune response |
|
|
383 | (1) |
|
Vaccination can inadvertently cause disease |
|
|
384 | (1) |
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The need for a vaccine and the demands placed on it change with the prevalence of the disease |
|
|
385 | (2) |
|
Vaccines have yet to be found for many chronic pathogens |
|
|
387 | (2) |
|
Genome sequences of human pathogens open up new avenues of vaccine design |
|
|
389 | (1) |
|
A useful vaccine against HIV has yet to be found |
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390 | (1) |
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|
390 | (1) |
|
Transplantation of tissues and organs |
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|
391 | (1) |
|
Transplant rejection and graft-versus-host reaction are immune responses caused by genetic differences between transplant donor and recipient |
|
|
391 | (1) |
|
In blood transfusion, donors and recipients are matched for the A,B,O system of blood group antigens |
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|
392 | (2) |
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Antibodies against A,B,O or HLA antigens cause hyperacute rejection of transplanted organs |
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|
394 | (1) |
|
Anti-HLA antibodies can arise from pregnancy, blood transfusion, or previous transplants |
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|
394 | (1) |
|
Organ transplantation involves procedures that inflame the donated organ and the transplant recipient |
|
|
395 | (1) |
|
Acute rejection is caused by effector T cells responding to HLA differences between donor and recipient |
|
|
396 | (1) |
|
Chronic rejection of organ transplants is due to the indirect pathway of allorecognition |
|
|
397 | (3) |
|
Matching donor and recipient for HLA class I and class II allotypes improves the outcome of transplantation |
|
|
400 | (1) |
|
Allogeneic transplantation is made possible by the use of immunosuppressive drugs |
|
|
400 | (1) |
|
Corticosteroids change patterns of gene expression |
|
|
401 | (2) |
|
Cytotoxic drugs kill proliferating cells |
|
|
403 | (1) |
|
Cyclosporin A, tacrolimus, and rapamycin selectively inhibit T-cell activation |
|
|
404 | (2) |
|
Antibodies specific for T cells are used to control acute rejection |
|
|
406 | (1) |
|
Patients needing a transplant outnumber the available organs |
|
|
407 | (1) |
|
Bone marrow transplantation is a treatment for genetic diseases of blood cells |
|
|
408 | (1) |
|
The alloreactions in bone marrow transplantation attack the patient, not the transplant |
|
|
409 | (2) |
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The impact of alloreactions on transplantation depends on the type of tissue or organ transplanted |
|
|
411 | (1) |
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|
411 | (1) |
|
Cancer and its interactions with the immune system |
|
|
412 | (1) |
|
Cancer results from mutations that cause uncontrolled cell growth |
|
|
412 | (2) |
|
A cancer arises from a single cell that has accumulated multiple mutations |
|
|
414 | (1) |
|
Exposure to chemicals, radiation, and viruses can facilitate the progression to cancer |
|
|
415 | (2) |
|
The immune system is insensitive to emerging cancer |
|
|
417 | (1) |
|
Allogeneic bone marrow transplantation is the preferred treatment for many cancer patients |
|
|
417 | (1) |
|
Patients receiving an HLA-identical bone marrow transplant can still get GVHD |
|
|
418 | (2) |
|
Some GVHD helps engraftment and prevents relapse of malignant disease |
|
|
420 | (1) |
|
NK cells can also mediate GVL effects |
|
|
420 | (1) |
|
Cancer cells continue to acquire mutations throughout the cancer's lifetime |
|
|
421 | (2) |
|
Vaccination with tumor antigens can produce regression of cancer |
|
|
423 | (2) |
|
Tumors frequently evade immunity by downregulation of HLA class I |
|
|
425 | (1) |
|
Heat-shock proteins can provide natural adjuvants of tumor immunity |
|
|
426 | (1) |
|
Vaccination against oncogenic viruses |
|
|
427 | (1) |
|
Monoclonal antibodies against cell-surface tumor antigens can be used for diagnosis and immunotherapy |
|
|
428 | (2) |
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|
|
429 | (1) |
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|
429 | (1) |
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|
430 | |
