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PART I DEVELOPMENT AND STRUCTURE OF MUCOSAL TISSUE |
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1 | (53) |
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Chapter 1 Overview of the Mucosal Immune System Structure |
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1 | (18) |
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Immune inductive lymphoid tissue |
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1 | (1) |
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1-1 MALT is different from lamina propria or glandular stroma |
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2 | (1) |
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1-2 The mucosal immune system contains different types of GALT |
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3 | (2) |
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1-3 Organogenesis of murine PPs, isolated lymphoid follicles, and NALT is not synchronous |
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5 | (1) |
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1-4 Lymphoid tissue is present in the nasopharynx and bronchi |
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6 | (1) |
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1-5 Mucosal B cells may be derived from tissues other than MALT |
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7 | (1) |
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B-cell activation in MALT |
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8 | (1) |
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1-6 FAE is an important site of antigen uptake in the gut |
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8 | (1) |
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1-7 Gut bacteria are important for the molecular interactions needed for germinal center formation |
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9 | (2) |
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B-cell differentiation in MALT germinal centers |
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11 | (1) |
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1-8 IgA expression and class switching are dependent on activation-induced cytidine deaminase (AID) |
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11 | (1) |
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1-9 Different class-switching pathways operate in different mucosal sites |
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12 | (1) |
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How mucosal immune cells home |
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13 | (1) |
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1-10 Naive and activated immune cells occupy different microenvironments in GALT |
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13 | (2) |
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1-11 Homing molecules are important in homing of cells to extraintestinal sites |
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15 | (4) |
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17 | (1) |
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18 | (1) |
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Chapter 2 Phylogeny of the Mucosal Immune System |
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19 | (8) |
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Phylogeny of receptor diversity |
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19 | (1) |
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2-1 T-cell receptors are similar in all jawed vertebrates |
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20 | (1) |
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2-2 Immunoglobulins have evolved in different ways in different lineages |
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20 | (1) |
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2-3 T and B cells are present in lower vertebrates |
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20 | (2) |
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The phylogeny of lymphoid tissue |
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22 | (1) |
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2-4 The lymphoid tissues in agnathans seem to have evolved from MALT |
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22 | (1) |
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2-5 Gnathostome lymphoid tissues differ between lineages |
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22 | (2) |
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The phylogeny of mucosal antibodies |
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24 | (1) |
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2-6 Immunoglobulin A is the secretory antibody in amniotes |
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24 | (1) |
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2-7 Amphibians have a unique antibody, immunoglobulin X |
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25 | (1) |
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2-8 Teleosts have a unique secretory antibody, IgT |
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25 | (2) |
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26 | (1) |
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26 | (1) |
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Chapter 3 Immunological and Functional Differences Between Individual Compartments of the Mucosal Immune System |
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27 | (10) |
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Common and distinct features of the mucosal immune system in different tissues |
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28 | (1) |
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3-1 The ocular immune system contains inductive sites |
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28 | (1) |
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3-2 In the oral cavity, SIgA dominates and sublingual tissue is a potential inductive site |
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28 | (1) |
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3-3 The upper and lower respiratory tract display discordant immunological features |
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29 | (1) |
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3-4 The upper and lower intestinal tract are the major source of Ig and the major site for the induction of immune responses |
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30 | (1) |
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3-5 Mammary glands are an important source of SIgA |
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31 | (1) |
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3-6 IgG is the major Ig in urogenital tract secretions |
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31 | (6) |
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Antigen sampling in mucosal surfaces |
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32 | (1) |
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B-cell subsets in nasal and gut-associated tissues |
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33 | (1) |
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33 | (1) |
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Influence of aging on mucosal immunity |
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34 | (1) |
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35 | (1) |
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36 | (1) |
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Chapter 4 Secreted Effectors of the Innate Mucosal Barrier |
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37 | (17) |
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The intestinal epithelium: stem cells, self-renewal, and cell lineage allocation |
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38 | (1) |
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4-1 Wnt signaling regulates intestinal epithelial cell positioning and differentiation |
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39 | (1) |
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4-2 Notch signaling determines cell lineage specification In the intestine |
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40 | (1) |
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Secretory cells in mucosal epithelia |
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41 | (1) |
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4-3 Nonspecialized epithelial cells display remarkable plasticity |
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41 | (1) |
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4-4 Mucus-producing cells are abundant in the gastrointestinal epithelium |
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41 | (1) |
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4-5 Antimicrobial peptides are produced by specialized cells throughout the gastrointestinal tract |
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42 | (1) |
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Biophysical features of the secreted mucus barrier |
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42 | (1) |
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4-6 Mucin glycoproteins have common structural features |
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43 | (1) |
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4-7 Mucin release is a tightly regulated biological process |
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43 | (1) |
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4-8 Antimicrobial peptides play a key role in mucosal defense |
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44 | (3) |
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Role of mucosal cell products in mucosal microbe homeostasis |
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47 | (1) |
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4-9 Microbes influence the composition and structure of the secreted mucosal barrier |
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47 | (1) |
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4-10 The secreted mucosal barrier influences the composition of the gut microbiome |
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48 | (1) |
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4-11 Mucins and Paneth cell products contribute to protection against infectious pathogens |
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48 | (6) |
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Regulation of the secreted mucosal barrier by innate and adaptive immunity |
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49 | (1) |
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Defects in mucosal barrier secretion and the pathogenesis of disease |
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50 | (1) |
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51 | (1) |
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51 | (3) |
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PART II CELLULAR CONSTITUENTS OF MUCOSAL IMMUNE SYSTEMS AND THEIR FUNCTION IN MUCOSAL HOMEOSTASIS |
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54 | (178) |
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Chapter 5 Immune Function of Epithelial Cells |
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55 | (14) |
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55 | (1) |
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5-1 Stratified squamous and simple columnar epithelia form the major types of epithelial structures |
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55 | (1) |
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5-2 A polarized simple epithelium permits vectorial transport |
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56 | (1) |
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5-3 Epithelial cells form a paracellular barrier via intercellular junctions |
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57 | (1) |
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5-4 Various types of differentiated epithelial cells are derived from an epithelial stem cell |
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58 | (1) |
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5-5 Nonimmunologic and innate factors contribute to epithelial barrier function |
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59 | (1) |
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5-6 Adaptive immunologic factors contribute to epithelial barrier function |
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60 | (1) |
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5-7 Inappropriate barrier function leads to mucosal pathology |
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60 | (1) |
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Antigen uptake and presentation |
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61 | (1) |
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5-8 Three major mechanisms account for regulated antigen uptake across the epithelium |
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61 | (1) |
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5-9 The epithelium exerts important innate immune functions |
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62 | (1) |
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5-10 The epithelium can present antigen via classical and nonclassical antigen-processing and antigen-presentation pathways |
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63 | (1) |
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5-11 The epithelium can provide co-stimulatory and tertiary cytokine signals to lymphocytes |
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64 | (1) |
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Regulation of immune responses |
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65 | (1) |
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5-12 Epithelial cells act as central organizers of immune responses |
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65 | (1) |
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5-13 Epithelial cells act as bystanders and participants in immune responses and inflammation |
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66 | (3) |
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68 | (1) |
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68 | (1) |
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Chapter 6 Intraepithelial Lymphocytes: Unusual T Cells at Epithelial Surfaces |
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69 | (18) |
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Uniqueness and heterogeneity of mucosal IELs |
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69 | (1) |
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6-1 Natural IELs are a unique cell type absent from the rest of the body |
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70 | (1) |
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6-2 Induced IELs are the mucosal counterpart of T cells found in the periphery |
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71 | (1) |
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6-3 Luminal factors control the numbers of IELs |
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71 | (1) |
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The TCR repertoire and specificity of IELs |
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72 | (1) |
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6-4 The TCR repertoire and antigen specificity of TCRγδ nIELs are different from T cells in the rest of the body |
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72 | (1) |
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6-5 TCRαβ IELs are highly unusual in that they are made up of a few dominant clones |
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73 | (1) |
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Development and differentiation of IELs |
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74 | (1) |
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6-6 Thymic versus extrathymic development of IELs is controversial |
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74 | (1) |
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6-7 Under euthymic normal conditions, all IEL subsets are progeny of bone marrow precursor cells that initially develop in the thymus |
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74 | (1) |
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6-8 Natural IEL precursor cells migrate directly from the thymus to the epithelium |
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75 | (1) |
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6-9 Cytokines and transcription factors are involved in the development and differentiation of TCRγδ nIELs |
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75 | (1) |
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6-10 CD8ααTCRαβ nIELs with self-reactivity may be positively selected |
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76 | (1) |
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6-11 iIELs are peripheral-antigen-driven progeny of conventional thymically selected CD4+ or CD8αβ+TCRαβ T lymphocytes |
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77 | (1) |
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Migration to and local adaptation in the gut |
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77 | (1) |
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6-12 Natural IELs are induced to home to the gut in the thymus |
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77 | (1) |
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6-13 Natural IELs undergo local adaptation in the gut |
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77 | (1) |
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6-14 Conventional thymically selected naive T cells are not found in the gut epithelium |
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78 | (1) |
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6-15 Induced IELs undergo adaptation in the gut |
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79 | (1) |
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The beneficial functions of IELs |
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80 | (1) |
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6-16 The function of nIELs appears to be to maintain epithelial homeostasis |
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80 | (1) |
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6-17 The functions of CD8ααTCRαβ nIELs remain largely unknown |
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80 | (2) |
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6-18 TCRαβCD8αβ iIELs appear to have a protective function |
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82 | (1) |
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6-19 TCRαβ CD4 iIELs are involved in protective immunity |
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83 | (1) |
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Potential aberrant function of IELs in inflammation |
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84 | (1) |
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6-20 TCRγδ nIELs may be involved in pathology |
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84 | (1) |
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6-21 CD8ααTCRαβ nIELs may also damage the epithelium |
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84 | (1) |
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6-22 CD8αβTCRαβ iIELs may be involved in the pathogenesis of inflammatory bowel disease |
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84 | (1) |
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6-23 Aberrant functions of CD4 TCRαβ iIELs driving gut inflammation |
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85 | (2) |
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85 | (1) |
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86 | (1) |
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Chapter 7 Lymphocyte Populations Within the Lamina Propria |
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87 | (16) |
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The origin and phenotype of mucosal T cells |
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88 | (1) |
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7-1 Mucosal T cells traffic from MALT to mucosal lamina propria |
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89 | (1) |
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7-2 Lamina propria T cells have the characteristics of activated lymphocytes |
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89 | (1) |
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7-3 Cytokine production by mucosal T cells in healthy animals is TH1/TH17 dominated |
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90 | (1) |
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7-4 IL-17 and IL-22 may play an important role in protecting mucosal surfaces |
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90 | (1) |
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7-5 Different types of gut microbiota appear to induce different cytokine responses in mucosal T cells |
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91 | (1) |
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7-6 The developmental pathways of TH17 cells are not well defined, especially at mucosal surfaces |
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92 | (1) |
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7-7 The role of local differentiation or selective migration in TH1 and TH17 responses is unclear |
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93 | (1) |
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7-8 The TH17 lineage displays considerable flexibility |
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94 | (2) |
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Regulatory T cells and the control of effector T-cell responses |
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96 | (1) |
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7-9 Human diseases due to single gene defects are informative in understanding gut inflammation and immune regulation |
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96 | (1) |
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7-10 Regulation of mucosal immune responses is complex and depends on whether the effector T cell can be regulated |
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97 | (6) |
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T cell-mediated gut diseases |
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98 | (1) |
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99 | (1) |
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100 | (1) |
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101 | (2) |
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Chapter 8 Mucosal B Cells and Their Function |
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103 | (18) |
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Cells and proteins involved in humoral immunity at mucosal surfaces |
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103 | (1) |
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8-1 MALT has major differences from conventional lymphoid tissue |
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104 | (3) |
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8-2 IgA and IgM are the dominant mucosal immunoglobuiins |
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107 | (2) |
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108 | (1) |
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8-3 IgA responses in MALT germinal centers are T-cell dependent |
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109 | (1) |
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8-4 A high level of somatic hypermutation characterizes mucosal B-cell responses |
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109 | (3) |
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8-5 Class-switch recombination generates IgA |
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112 | (1) |
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8-6 Chemokines and chemokine receptors are involved in the organization of MALT and germinal centers |
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113 | (2) |
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8-7 The exit of activated B cells from germinal centers is controlled by various factors |
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115 | (1) |
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8-8 IgA responses can occur in the absence of cognate B cell---T cell interaction |
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115 | (2) |
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The instructions involved in inducing GALT B cells to migrate to effector sites |
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116 | (1) |
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B-lineage activity in the lamina propria-current controversies |
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116 | (1) |
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8-9 The activation of mucosal B cells and their maturation to IgA-producing plasma cells outside of GALT is controversial |
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117 | (1) |
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8-10 Evidence indicates that the switch event to human IgA1 or IgA2 production can occur outside of GALT |
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117 | (1) |
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8-11 B cells in the gut lamina propria do not divide before plasma cell differentiation |
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118 | (3) |
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118 | (1) |
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119 | (2) |
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Chapter 9 Secretory Immunoglobuiins and Their Transport |
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121 | (20) |
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Features of secretory immunoglobuiins |
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121 | (1) |
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9-1 The relative distribution and molecular forms of Ig isotypes in external secretions display marked differences in comparison with plasma |
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121 | (4) |
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9-2 The distribution of mucosal immunoglobuiins differs between species |
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125 | (1) |
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9-3 The biosynthesis of mucosal IgA is distinct from circulating IgA |
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125 | (1) |
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9-4 IgA exists as two subclasses, IgA1 and IgA2 |
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126 | (1) |
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9-5 IgA is heavily glycosylated with important functional consequences |
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127 | (1) |
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9-6 J chain is a unique protein that links together monomeric IgA to create polymeric IgA |
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127 | (1) |
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Epithelial transcytosis of secretory immunoglobuiins |
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128 | (1) |
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9-7 The polymeric immunoglobulin receptor delivers polymeric IgA and IgM into mucosal secretions |
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128 | (2) |
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9-8 Expression of pIgR by mucosal epithelial cells is regulated by microbial and host factors |
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130 | (1) |
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9-9 Bidirectional transport of IgG and IgE across mucosal epithelia is mediated by specialized Fc receptors |
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131 | (3) |
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Functions of mucosal immunoglobuiins |
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134 | (1) |
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9-10 Secretory Igs protect mucosal surfaces against microbial invasion |
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134 | (1) |
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9-11 Epithelial transcytosis of mucosal Igs enhances immune defense |
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135 | (1) |
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9-12 SIgA and secretory component possess innate immune functions through their carbohydrate modifications and regulate mucosal inflammation |
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136 | (1) |
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9-13 Mucosal Igs also interact with Fc receptors on immune cells |
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136 | (1) |
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Strategies employed by pathogens to evade IgA-mediated defense |
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137 | (1) |
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9-14 Pathogens express IgA1 proteases that destroy IgA function |
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137 | (1) |
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9-15 Pathogenic bacteria express binding proteins specific for IgA and secretory component that are involved in virulence |
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138 | (3) |
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139 | (1) |
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139 | (2) |
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Chapter 10 Role of Dendritic Cells in Integrating Immune Responses to Luminal Antigens |
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141 | (18) |
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Defining characteristics of dendritic cells |
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141 | (1) |
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10-1 Dendritic cells capture antigens and select and activate naive T-cell clones in vivo |
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142 | (1) |
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10-2 Dendritic cells determine the nature of lymphocyte responses |
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142 | (1) |
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10-3 Dendritic cells are a family of cells with distinct subpopulations |
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143 | (2) |
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10-4 Dendritic cell function is influenced by activation signals |
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145 | (1) |
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Intestinal dendritic cell populations |
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145 | (1) |
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10-5 Distinct populations of dendritic cells are present in mucosal inductive and effector sites and capture antigens by different mechanisms |
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145 | (3) |
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Unique functions of intestinal dendritic cells |
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148 | (1) |
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10-6 Oral tolerance is mediated by intestinal CD103+ dendritic cells and resident dendritic cells in the spleen and lymph nodes |
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148 | (1) |
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10-7 Dendritic cells regulate T-cell responses to intestinal bacteria |
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149 | (2) |
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10-8 DCs are essential for both T-cell dependent and independent IgA B-cell responses in the intestine |
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151 | (1) |
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10-9 DCs drive intestinal homing receptors on T cells and B cells through their production of RA |
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152 | (1) |
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Dendritic cell conditioning |
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152 | (1) |
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10-10 DCs are conditioned by the local microenvironment |
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153 | (1) |
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Role of mucosal dendritic cells in IBD |
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154 | (1) |
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10-11 Intestinal dendritic cells in mice with experimental colitis display impaired induction of Treg cells and enhanced induction of TH1 and TH17 cell differentiation |
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154 | (1) |
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10-12 DCs are activated in the intestinal mucosa in IBD |
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155 | (4) |
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156 | (1) |
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156 | (3) |
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Chapter 11 Intestinal Macrophages in Defense of the Mucosa |
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159 | (12) |
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Origin of lamina propria macrophages |
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159 | (1) |
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11-1 Mucosal macrophages are derived from pluripotent stem cells in the bone marrow |
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160 | (1) |
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11-2 Blood monocytes continually populate the lamina propria of the uninflamed healthy intestinal mucosa |
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161 | (1) |
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11-3 Blood monocytes are the predominant source of macrophages in inflammatory lesions in intestinal mucosa |
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162 | (2) |
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Role of lamina propria macrophages in intestinal homeostasis |
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163 | (1) |
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11-4 Intestinal macrophages are uniquely inflammation anergic |
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164 | (1) |
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11-5 Inflammation anergy of intestinal macrophages is due to inactive NFκB signaling |
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165 | (1) |
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11-6 Active TGF-β/Smad signaling contributes to inflammation anergy of intestinal macrophages |
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166 | (1) |
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11-7 Macrophages do not present antigen in normal intestinal mucosa |
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167 | (1) |
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11-8 Murine intestinal macrophages have immunoregulatory function |
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168 | (1) |
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Intestinal macrophages in host defense |
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168 | (1) |
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11-9 Intestinal macrophages scavenge apoptotic cells |
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168 | (1) |
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11-10 Intestinal macrophages participate in host defense against mucosal pathogens |
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168 | (3) |
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169 | (1) |
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170 | (1) |
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Chapter 12 Mucosal Basophils, Eosinophils, and Mast Cells |
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171 | (20) |
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171 | (1) |
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12-1 Basophils arise from a common granulocyte-monocyte precursor in the bone marrow |
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172 | (1) |
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12-2 Basophils provide effector functions by releasing preformed mediators as a consequence of IgE-dependent and IgE-independent stimuli |
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172 | (1) |
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12-3 The effector functions of basophils can be activated by IgE, IgG1, and IgD antibody-antigen complexes |
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172 | (1) |
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12-4 Basophils are activated by cytokines such as IL-3, IL-18, and IL-33 |
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173 | (1) |
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12-5 Basophils can sense microbial products to provide innate immune resistance |
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174 | (1) |
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12-6 Basophils are activated by Toll-like and complement receptors for innate immune function |
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174 | (1) |
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12-7 Basophils are recruited to inductive and effector sites throughout an immune response |
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174 | (1) |
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12-8 Basophils possess antigen-presenting functions and cooperate with dendritic cells in the induction of TH2 immunity along mucosal surfaces |
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175 | (1) |
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Biology of mucosal eosinophils |
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176 | (1) |
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12-9 Development of eosinophils depends on lineage-specific transcription factors and cytokines |
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176 | (1) |
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12-10 Eosinophil survival and recruitment are largely determined by IL-5 and eotaxin |
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177 | (1) |
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12-11 Eosinophils are activated by a broad array of signals and function primarily through their ability to secrete a wide range of soluble mediators |
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177 | (1) |
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12-12 Mucosal eosinophils collaborate with epithelial cells, T cells, mast cells, and nerve cells in mucosal immunophysiology |
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178 | (2) |
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179 | (1) |
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12-13 Mast cells develop from immature bone marrow derived precursors in mucosal tissues |
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180 | (1) |
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12-14 Mast cell effector function is initiated by IgE-dependent and IgE-independent stimuli |
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181 | (2) |
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12-15 Mast cells exert their biological functions almost exclusively by secretion of humoral factors |
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183 | (1) |
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12-16 Mucosal mast cells respond to extrinsic and intrinsic signals and thus regulate the function of the mucosal barrier and smooth muscle motor function |
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183 | (1) |
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12-17 Mast cells provide host defense against microbes |
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184 | (1) |
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12-18 Mast cells not only induce an immune response and inflammation but also regulate the immune response and the resultant processes of tissue repair |
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185 | (1) |
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Mucosal basophils, eosinophils, and mast cells in human disease |
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186 | (1) |
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12-19 Mucosal basophils are involved in allergies of the skin and intestines, asthma, and autoimmunity |
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186 | (1) |
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12-20 Mucosal eosinophils are associated with asthma, parasitic and viral infections, mucosal allergy, and several hypereosinophilic disorders that are characterized by mucosal infiltration with eosinophils |
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186 | (2) |
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12-21 Mucosal mast cells are important mediators of the inflammation associated with allergy, asthma, celiac disease, inflammatory bowel disease, and diseases of unknown origin such as irritable bowel syndrome and systemic mastocytosis |
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188 | (3) |
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190 | (1) |
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190 | (1) |
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Chapter 13 M Cells and the Follicle-Associated Epithelium |
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191 | (14) |
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191 | (1) |
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13-1 FAE promotes antigen sampling |
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191 | (1) |
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13-2 FAE attracts specific populations of DCs and lymphocytes into organized mucosal lymphoid tissues |
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192 | (1) |
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M cells as gateways to the mucosal immune system |
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193 | (1) |
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13-3 M cells are polarized epithelial cells with unique architecture |
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193 | (1) |
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13-4 The M cell apical surface is designed for easy access and efficient endocytosis |
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194 | (1) |
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13-5 M cells display cell type-specific membrane molecules that may serve as receptors |
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195 | (1) |
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13-6 Adherent macromolecules and particles are efficiently endocytosed and transported across M cells |
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195 | (1) |
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13-7 Transported cargo is delivered to cells in the M-cell pocket and subepithelial dome region |
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196 | (2) |
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Formation, differentiation, and maintenance of the FAE and M cells |
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198 | (1) |
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13-8 FAE is continuously renewed |
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198 | (1) |
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13-9 Signals from organized mucosal lymphoid tissues are required for induction of FAE and M cells |
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198 | (1) |
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13-10 New organized mucosal lymphoid tissue and FAE form in response to antigenic challenge |
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199 | (1) |
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Exploitation of M cells by microorganisms |
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199 | (1) |
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13-11 M-cell transport of noninvasive, surface-colonizing bacterial pathogens can limit the duration of diarrheal disease |
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200 | (1) |
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13-12 Invasive bacterial pathogens can exploit rapid M-cell transport to establish local and systemic infection |
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200 | (1) |
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13-13 Endocytosis of viruses by M cells results in mucosal and/or systemic disease |
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201 | (1) |
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13-14 M cells can be exploited for vaccine antigen delivery |
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202 | (3) |
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203 | (1) |
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203 | (2) |
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Chapter 14 Lymphocyte Trafficking from Inductive Sites to Effector Sites |
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205 | (14) |
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Basic concepts in immune-cell migration |
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206 | (1) |
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14-1 The adhesion molecules and chemoattractants involved in immune-cell migration |
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206 | (1) |
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14-2 Immune-cell migration into tissues is a multi-step process |
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207 | (2) |
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14-3 Naive lymphocytes recirculate through MALT |
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209 | (1) |
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14-4 Lymphocytes traffic inside lymph nodes and leave to return to the blood |
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210 | (2) |
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Lymphocyte migration into mucosal tissues---generation of tissue-tropic lymphocyte subsets |
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212 | (1) |
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14-5 Specific integrin-adhesion-molecule interactions and chemokines direct cell migration into mucosal tissues |
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212 | (1) |
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14-6 Lymphocytes usually remain in tissues, but some reenter the circulating pool |
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213 | (1) |
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14-7 Different homing molecules control lymphocyte migration to gut and skin |
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214 | (1) |
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14-8 Dendritic cells are critical in the generation of tissue-tropic effector lymphocyte subsets |
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215 | (1) |
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14-9 Vitamin A is required for the generation of gut-tropic effector T lymphocytes |
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216 | (3) |
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Lymphocyte migration to sites of mucosal inflammation---therapeutic opportunities |
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217 | (1) |
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218 | (1) |
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218 | (1) |
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Chapter 15 Mucosal Tolerance |
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219 | (13) |
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General features of mucosal tolerance |
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219 | (2) |
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15-1 Mucosal tolerance involves many mechanisms including anergy, deletion, and the induction of active regulatory pathways |
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221 | (1) |
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15-2 Mucosal tolerance is likely induced in organized lymphoid structures associated with mucosal tissues and is disseminated widely throughout the MALT |
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222 | (1) |
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15-3 A wide variety of immune effector functions are subject to the effects of mucosal tolerance, which can be enhanced by mucosal adjuvants |
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222 | (2) |
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Mucosal tolerance in experimental autoimmune and inflammatory disease |
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223 | (1) |
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15-4 Mucosal tolerance can be elicited to autoantigens in experimental model systems |
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224 | (1) |
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15-5 The mechanisms of mucosal tolerance that are induced in response to autoantigens are similar to those induced against model antigens |
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225 | (1) |
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Oral tolerance in the treatment of human immune-mediated diseases |
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226 | (1) |
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15-6 Mucosal (oral) tolerance is a property of normal human mucosal tissues |
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226 | (1) |
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15-7 Mucosal tolerance may be amenable to therapeutic manipulation in human immune-mediated disease |
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227 | (1) |
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15-8 Mucosal tolerance can be used in the treatment of human allergic disorders |
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228 | (4) |
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229 | (1) |
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229 | (3) |
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PART III MICROBIAL COMMENSALISM |
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232 | (30) |
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Chapter 16 Recognition of Microbe-Associated Molecular Patterns by Pattern Recognition Receptors |
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233 | (12) |
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Principles of pattern recognition and signaling |
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234 | (1) |
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16-1 TLRs comprise a family of conserved receptors that recognize specific PAMPs |
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234 | (2) |
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16-2 NOD1 and NOD2 are NLR family members that recognize peptidoglycan motifs |
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236 | (1) |
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16-3 TLR and NOD signaling pathways converge on downstream NFκB and MAPK |
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237 | (1) |
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Function of pattern recognition molecules in healthy mucosa |
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238 | (1) |
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16-4 Negative regulation prevents prolonged and detrimental TLR/NOD signaling |
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238 | (1) |
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16-5 TLR function is involved in the maintenance of mucosal barrier integrity |
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239 | (1) |
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16-6 NOD2 modulates antimicrobial peptide secretion and bacterial clearance via autophagy |
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240 | (1) |
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Genetic alterations in pattern recognition |
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241 | (1) |
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16-7 NOD2 is a major susceptibility gene for Crohn's disease |
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241 | (1) |
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16-8 TLR polymorphisms may modulate IBD severity |
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242 | (3) |
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243 | (1) |
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243 | (2) |
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Chapter 17 The Commensal Microbiota and Its Relationship to Homeostasis and Disease |
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245 | (1) |
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Principles and definitions of the commensal microbiota |
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246 | (1) |
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The microbial communities at mucosal surfaces |
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247 | (1) |
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17-1 The upper respiratory microbiome of the nares is distinctive with similar phyla between individuals |
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248 | (1) |
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17-2 The oral microbiome is characterized by the formation of biofilms |
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248 | (1) |
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17-3 The gut microbiome is the most complex of the commensal ecosystems of the host |
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249 | (1) |
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Host-microbe interactions |
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250 | (1) |
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17-4 The host perceives and responds to the microbiota |
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250 | (1) |
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17-5 Life without microbiota results in profound changes in the host |
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251 | (1) |
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17-6 T-cell responses appear to be modulated by the microbiota |
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252 | (1) |
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17-7 Segmented filamentous bacteria specifically drive TH17 responses |
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252 | (1) |
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17-8 The intestinal microbiota influences autoimmunity |
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253 | (2) |
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17-9 The microbiota appears to be involved in inflammatory bowel disease, particularly Crohn's disease |
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255 | (1) |
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17-10 Defective immune system handling of intestinal microbes leads to intestinal inflammation |
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256 | (2) |
|
Influence of microbiota on host metabolism |
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|
257 | (1) |
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17-11 Alterations in the community structure of colonic microbes are linked to obesity and the metabolic syndrome |
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|
258 | (1) |
|
17-12 The host genome interacts with the microbiome to influence host phenotype |
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259 | (3) |
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260 | (1) |
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260 | (2) |
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PART IV GENITOURINARY TRACT |
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262 | (30) |
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Chapter 18 The Immune System of the Genitourinary Tract |
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263 | (12) |
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Anatomy of the human male and female reproductive tract |
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|
263 | (1) |
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Hormonal regulation of female reproductive function |
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264 | (1) |
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18-1 Cytokines, chemokines, and antimicrobial products contribute to protection of the female reproductive tract |
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|
264 | (2) |
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18-2 Cellular immunity is also important in the reproductive tract |
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|
266 | (1) |
|
Endocrine control of immune protection in the reproductive tract |
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|
267 | (1) |
|
18-3 Sex hormones directly and indirectly regulate immune-cell function in the reproductive tract |
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|
267 | (1) |
|
18-4 Immune protection is integrated in the female reproductive tract during the menstrual cycle |
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|
268 | (1) |
|
18-5 Immune mechanisms contribute to protection of the male reproductive tract |
|
|
268 | (1) |
|
18-6 Innate immunity is an important component of the male reproductive tract immune system |
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|
269 | (1) |
|
18-7 Adaptive immunity in the male reproductive tract is mediated predominantly by CD8+ T cells |
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|
270 | (1) |
|
Infection and immune protection against sexually transmitted diseases in the male and female reproductive tract |
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|
271 | (1) |
|
18-8 Chlamydia trachomatis is the most common sexually transmitted disease worldwide |
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|
271 | (4) |
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|
273 | (1) |
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|
273 | (2) |
|
Chapter 19 Mucosal Immune Responses to Microbes in the Genital Tract |
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|
275 | (17) |
|
Global prevalence of sexually transmitted pathogens |
|
|
275 | (1) |
|
Diseases caused by sexually transmitted pathogens |
|
|
276 | (1) |
|
19-1 Chlamydia is a disease caused by the bacteria Chlamydia trachomatis |
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|
276 | (1) |
|
19-2 Gonorrhea is an STD that is caused by a bacterium, Neisseria gonorrhoeae |
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|
276 | (1) |
|
19-3 Syphilis is caused by infection with the bacterium Treponema pallidum |
|
|
276 | (1) |
|
19-4 Trichomonas vaginalis, the cause of trichomoniasis, is a protozoal parasite that infects the vagina |
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|
277 | (1) |
|
19-5 Human immunodeficiency virus 1 (HIV-1), the cause of acquired immunodeficiency syndrome (AIDS), is an STD |
|
|
277 | (1) |
|
19-6 Genital herpes is caused by infection with herpes simplex virus-2 (HSV-2) and, less commonly, HSV-1 |
|
|
277 | (1) |
|
19-7 Human papillomavirus (HPV) infects the stratified squamous epithelium |
|
|
277 | (1) |
|
19-8 Hepatitis B virus (HBV) is a hepatotropic virus that is transmitted through sexual contact |
|
|
278 | (1) |
|
Invasion mechanisms employed by sexually transmitted pathogens |
|
|
278 | (1) |
|
19-9 Chlamydia exhibits distinct infectious (elementary body) and replicative forms (reticulate body) |
|
|
278 | (1) |
|
19-10 Gonorrhea infects the apical surface of simple columnar epithelium and once invaded inhibits the function of the adaptive immune system |
|
|
279 | (1) |
|
19-11 Treponema pallidum invades humans at mucosal epithelia where it causes infection and gains access to the blood and lymph systems |
|
|
279 | (1) |
|
19-12 Trichomoniasis is initiated within either the female cervico-vaginal epithelium or the male urethral epithelium |
|
|
279 | (1) |
|
19-13 HIV-1 gains access to the immune system by crossing the epithelial cell barrier |
|
|
280 | (1) |
|
19-14 Genital herpes infection initially targets the stratified squamous epithelium |
|
|
280 | (1) |
|
19-15 HPV infection requires access to the basement membrane for infection of basal keratinocytes of stratified epithelium |
|
|
280 | (1) |
|
19-16 HBV is a mucosal pathogen in approximately one-third of infections in adults |
|
|
281 | (1) |
|
The innate immune system of the genital mucosa and its relation to infections |
|
|
281 | (1) |
|
19-17 Mucus is the first line of epithelial defense |
|
|
282 | (1) |
|
19-18 Female and male genitourinary secretions contain antimicrobial factors |
|
|
282 | (1) |
|
19-19 The female and male genitourinary systems possess an endogenous (commensal) microbiota that provides |
|
|
|
colonization resistance against pathogenic infections |
|
|
283 | (1) |
|
19-20 Innate immune cells provide defense against invading pathogens within the female and male genitourinary tract |
|
|
283 | (1) |
|
Innate recognition of sexually transmitted pathogens |
|
|
284 | (1) |
|
19-21 Chlamydia trachomatis is recognized by multiple PRRs |
|
|
284 | (1) |
|
19-22 Host cells utilize immunoglobulin-related molecules such as CEACAM3 to initiate internalization and elimination of Neisseria gonorrhoeae |
|
|
284 | (1) |
|
19-23 Treponema pallidum lacks lipopolysaccharide but contains internal lipoproteins which can stimulate Toll-like receptors |
|
|
285 | (1) |
|
19-24 Innate immune recognition of HIV-1 occurs after cellular infection |
|
|
285 | (1) |
|
19-25 Toll-related receptor and retinoic acid-inducible gene-related pattern recognition is involved in detecting genital herpes infection |
|
|
286 | (1) |
|
19-26 HPV infection is sensed by innate and adaptive immune cells through Toll-like receptors |
|
|
286 | (1) |
|
19-27 HBV impairs innate immune responses as a means of immune evasion |
|
|
287 | (1) |
|
Adaptive immune responses against sexually transmitted pathogens |
|
|
287 | (1) |
|
19-28 Chlamydia infection triggers the activation of local DCs to migrate to the draining lymph nodes and initiate T-cell activation |
|
|
288 | (1) |
|
19-29 TH1 cells mediate immunity against gonorrhea |
|
|
288 | (1) |
|
19-30 Protective immunity to syphilis is undefined but likely exists |
|
|
288 | (1) |
|
19-31 Immunity to Trichomonas infection involves both B- and T-cell responses |
|
|
288 | (1) |
|
19-32 Adaptive immunity is the mainstay of resistance to genital herpes infection |
|
|
288 | (1) |
|
19-33 HPV engenders limited immune responses leading to persistent, latent infection |
|
|
289 | (1) |
|
19-34 Cellular and humoral immunity is essential for immunity to HIV-1 |
|
|
289 | (1) |
|
19-35 Adaptive immunity is critical to limiting and resolving HBV infection |
|
|
289 | (3) |
|
|
|
290 | (1) |
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|
|
290 | (1) |
|
|
|
291 | (1) |
|
PART V NOSE, AIRWAYS, ORAL CAVITY, AND EYES |
|
|
292 | (50) |
|
Chapter 20 The Nasopharyngeal and Oral Immune System |
|
|
293 | (14) |
|
The nasopharyngeal-oral mucosal immune system |
|
|
293 | (1) |
|
20-1 The MALT of the gut and upper airway share features of antigen uptake |
|
|
294 | (1) |
|
20-2 NALT is a major IgA inductive site for the nasal and oral mucosa |
|
|
295 | (1) |
|
20-3 The nasal passage contains a new type of mucosal tissue |
|
|
296 | (1) |
|
20-4 The salivary glands have features of both secretory and systemic immunity |
|
|
297 | (2) |
|
Induction of acquired immune responses via the oral and nasal mucosal immune system |
|
|
299 | (1) |
|
20-5 Enterotoxin-based nasal adjuvants are the most effective method for the induction of antigen-specific immunity |
|
|
299 | (1) |
|
20-6 Safe mucosal adjuvants have been developed as delivery systems for nasal vaccines |
|
|
300 | (2) |
|
20-7 Nasal adjuvants activate the innate immune system |
|
|
302 | (1) |
|
20-8 The mouth is a delivery site for the induction and modification of antigen-specific immune responses |
|
|
303 | (1) |
|
20-9 The nasal immune system escapes mucosal aging |
|
|
304 | (1) |
|
20-10 T-cell independent mucosal IgA responses are induced in the nasal and oral cavities |
|
|
305 | (2) |
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|
|
305 | (1) |
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|
|
306 | (1) |
|
Chapter 21 Bronchus-Associated Lymphoid Tissue and Immune-Mediated Respiratory Diseases |
|
|
307 | (22) |
|
General anatomy and physiology of the central and lower airways |
|
|
307 | (1) |
|
21-1 BALT is a potential inductive site |
|
|
307 | (1) |
|
21-2 The airway mucosa contains effector sites that are similar to those in other mucosal tissues |
|
|
308 | (1) |
|
Response of the lung to environmental challenges |
|
|
309 | (1) |
|
21-3 Two major chronic inflammatory diseases of the lung are asthma and chronic obstructive pulmonary disease (COPD) |
|
|
309 | (1) |
|
21-4 The inflammation in COPD is characterized as either chronic bronchitis or emphysema |
|
|
309 | (1) |
|
21-5 Allergy is a central mechanism in the pathogenesis of asthma |
|
|
310 | (2) |
|
Characteristics of allergens |
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|
312 | (1) |
|
21-6 Allergens have intrinsic properties as defined by their ability to be directly recognized by specific receptors |
|
|
312 | (1) |
|
Role of innate immune cell types in the induction of asthma |
|
|
312 | (1) |
|
21-7 DCs and alveolar macrophages are the major APCs in asthma |
|
|
313 | (1) |
|
21-8 Mast cells, basophils, and eosinophils are the main innate immune cells that are recruited to the airways during asthma |
|
|
314 | (1) |
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|
|
315 | (1) |
|
21-9 The late-phase response of asthma is characterized by the infiltration of the airways with inflammatory cells |
|
|
315 | (1) |
|
21-10 Treg cells are also recruited or induced locally during asthma and provide restraint on the inflammatory response |
|
|
316 | (1) |
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|
|
316 | (1) |
|
21-11 Asthma is a complex genetic disease |
|
|
316 | (1) |
|
21-12 The marked increase in the prevalence of asthma supports the importance of environmental factors |
|
|
317 | (1) |
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|
|
318 | (1) |
|
21-13 Consistent with its genetic heterogeneity, asthma involves other pathways beyond the TH2 paradigm |
|
|
318 | (1) |
|
21-14 Innate pathways and their associated cytokines can initiate asthma |
|
|
319 | (1) |
|
Mediators involved in the development of asthma |
|
|
320 | (1) |
|
21-15 TSLP is a novel IL-17-like cytokine that promotes TH2-related immune responses |
|
|
320 | (1) |
|
21-16 IL-25 is an IL-17 cytokine family member that amplifies TH2 responses |
|
|
321 | (1) |
|
21-17 IL-33 is an IL-1 family member that enhances the activity of mast cells, basophils, and eosinophils |
|
|
322 | (1) |
|
21-18 IL-17 derived from TH17 cells and innate immune cells enhances neutrophilic responses in asthma |
|
|
322 | (1) |
|
21-19 IL-22 derived from TH2 cells promotes epithelial cell responses associated with the asthma phenotype |
|
|
323 | (1) |
|
Innate effector cells in the development of asthma |
|
|
323 | (1) |
|
21-20 Lung epithelial cells may have a central role in the induction and maintenance of asthma |
|
|
323 | (1) |
|
21-21 Natural helper cells/nuocytes are lymphoid tissue inducer (LTi)-like cells that initiate TH2-related inflammation |
|
|
324 | (1) |
|
21-22 Alternatively activated macrophages promote TH2 inflammation in asthma |
|
|
324 | (1) |
|
21-23 NKT cells have a central role in the initiation of the asthma phenotype in mouse models |
|
|
325 | (1) |
|
21-24 NKT cells may be central mediators of human asthma |
|
|
325 | (4) |
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|
|
326 | (1) |
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|
|
326 | (3) |
|
Chapter 22 The Ocular Surface as a Mucosal Immune Site |
|
|
329 | (13) |
|
Organization of the eye-associated lymphoid tissue |
|
|
330 | (1) |
|
22-1 The EALT contains organized and diffuse populations of lymphocytes |
|
|
331 | (1) |
|
22-2 The lacrimal gland and the lacrimal gland-associated lymphoid tissue are anatomically located within the upper eyelid |
|
|
331 | (1) |
|
22-3 Conjunctiva-associated lymphoid tissue (CALT) covers the external surface of the eye with three anatomic regions (palpebral, bulbar, and fornix) |
|
|
332 | (1) |
|
22-4 Tear-duct-associated lymphoid tissue (TALT) is present in rodents and humans and is subject to a pathway of organogenesis that is distinct from GALT |
|
|
333 | (2) |
|
Induction and expression of immunity at the ocular surface---the good and the bad |
|
|
334 | (1) |
|
22-5 Regulatory mechanisms exist in the EALT that restrict an inflammatory response |
|
|
335 | (1) |
|
22-6 Immunization through the ocular mucosal immune system can, however, induce an immune response |
|
|
336 | (1) |
|
Diseases associated with dysfunction of the ocular mucosal immune system |
|
|
336 | (1) |
|
22-7 Loss of tear fluid results in dry eye syndrome |
|
|
336 | (1) |
|
22-8 Sjogren's syndrome is an autoimmune disease of the lacrimal and salivary glands |
|
|
337 | (1) |
|
22-9 Ocular cicatricial pemphigoid is an autoimmune disease that is directed against components of the basement membrane |
|
|
338 | (1) |
|
22-10 Allergy is a common clinical manifestation in the eye due to its exposed surfaces |
|
|
338 | (1) |
|
22-11 Herpetic stromal keratitis is a pathologic response against the cornea after herpes virus infection has been cleared |
|
|
339 | (1) |
|
22-12 The interior of the eye is an immune privileged site due to powerful regulatory mechanisms that resist immune activation |
|
|
340 | (2) |
|
|
|
340 | (1) |
|
|
|
341 | (1) |
|
PART VI INFECTIOUS DISEASES OF MUCOSAL SURFACES |
|
|
342 | (88) |
|
Chapter 23 Mucosal Interactions with Enteropathogenic Bacteria |
|
|
343 | (20) |
|
The gastrointestinal epithelium: a physical and physiological barrier against bacteria |
|
|
344 | (1) |
|
23-1 The gastrointestinal epithelium acts as a sensor of luminal microbes and functions as an innate immune barrier |
|
|
344 | (1) |
|
23-2 The epithelium is a regulated gatekeeper for commensal bacteria |
|
|
345 | (2) |
|
The epithelium: a gateway for enteropathogens |
|
|
347 | (1) |
|
23-3 Some bacteria express fimbriae that allow for adhesion to the epithelium |
|
|
347 | (3) |
|
23-4 Adherent-invasive E. coli (AIEC) utilize fimbriae to adhere to CEACAM6 and invade epithelia |
|
|
350 | (2) |
|
23-5 Bacteria have developed a large number of nonpolymeric structures that participate in afimbrial adhesion to and/or invasion of host cells |
|
|
352 | (1) |
|
Beyond adhesion: bacterial injection systems |
|
|
353 | (1) |
|
23-6 At least six different (type I-VI) bacterial `injection' systems have been defined |
|
|
353 | (1) |
|
23-7 Bacteria-associated secretion systems inject specific bacterial effectors into the epithelium, which affects host membrane proteins and cytoskeleton |
|
|
354 | (2) |
|
Mechanisms of bacterially induced epithelial cell dysfunction |
|
|
355 | (1) |
|
23-8 Bacteria secrete toxins that affect epithelial cell function into the lumen of the intestines |
|
|
356 | (1) |
|
23-9 Bacteria use their secretion machinery to directly inject toxic effector molecules that co-opt epithelial function for the pathogen's benefit |
|
|
356 | (1) |
|
Regulation of host epithelial innate immune responses by bacteria |
|
|
357 | (1) |
|
23-10 Pathogenicity, in comparison with commensalism, is often determined by the structure-function relationships between microbial MAMPs and host PRRs |
|
|
357 | (1) |
|
23-11 Commensal and pathogenic microbiota engage PRRs in a distinctive manner |
|
|
357 | (2) |
|
23-12 Bacterial effectors from enteropathogens manipulate epithelial intracellular signaling cascades |
|
|
359 | (4) |
|
|
|
360 | (1) |
|
|
|
361 | (2) |
|
Chapter 24 Helicobacter pylori Infection |
|
|
363 | (14) |
|
H. pylori as commensal or pathogen |
|
|
364 | (1) |
|
24-1 H. pylori has coevolved with humans and persists for life |
|
|
364 | (1) |
|
24-2 Bacterial and host factors can prevent disease |
|
|
364 | (1) |
|
H. pylori virulence factors |
|
|
365 | (1) |
|
24-3 Flagellin mediates bacterial motility in gastric mucus |
|
|
365 | (1) |
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24-4 Urease enables bacterial survival and adhesion |
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365 | (1) |
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24-5 vacA encodes a cytotoxin that mediates long-term persistence |
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365 | (1) |
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24-6 The H. pylori cag pathogenicity island is a strain-specific locus that enhances the risk for disease |
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366 | (1) |
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24-7 Additional H. pylori determinants influence disease pathogenesis |
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367 | (1) |
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H. pylori and the innate immune system |
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368 | (1) |
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24-8 H. pylori interacts with epithelial Toll-like receptors |
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368 | (1) |
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24-9 Neutrophil accumulation is a characteristic feature of |
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H. pylori-infected mucosa |
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369 | (1) |
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24-10 Macrophages may contribute to inflammatory and carcinogenic responses to H. pylori |
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370 | (1) |
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24-11 Dendritic cells initiate the immune response to H. pylori |
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371 | (3) |
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Adaptive immune responses to H. pylori |
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373 | (1) |
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24-12 H. pylori induces a mixed T-cell response |
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374 | (1) |
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24-13 H. pylori infection induces a local and systemic antibody response that is not protective |
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374 | (1) |
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24-14 H. pylori infection may lead to B-cell transformation |
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375 | (2) |
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375 | (1) |
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375 | (2) |
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Chapter 25 Viral Infections |
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377 | (20) |
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377 | (1) |
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25-1 Rotavirus structure impacts pathogenicity in the Intestinal mucosa |
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378 | (1) |
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25-2 Rotavirus replicates in intestinal epithelial cells |
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379 | (1) |
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25-3 Rotavirus infection is calcium (Ca2+) dependent |
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380 | (1) |
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380 | (1) |
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25-4 Rotavirus virulence is mediated by five genes |
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381 | (1) |
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25-5 Diarrheal illness caused by rotavirus is multifactorial |
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381 | (1) |
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25-6 Mucosal rotavirus infection is associated with extraintestinal rotavirus |
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382 | (1) |
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382 | (1) |
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25-7 Multiple immune cells contribute to host responses to rotavirus |
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383 | (1) |
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25-8 Type I interferon responses contribute to rotavirus clearance |
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383 | (1) |
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384 | (1) |
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25-9 The first available rotavirus vaccine was a live attenuated vaccine |
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384 | (1) |
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25-10 Rotavirus is a vaccine-preventable enteric infection |
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384 | (1) |
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25-11 New rotavirus vaccines are under development |
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385 | (1) |
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385 | (1) |
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25-12 Mucosal surfaces mediate HIV-1 entry |
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386 | (1) |
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25-13 Cervico-vaginal mucosa provides both barrier function and pathways for HIV-1 entry |
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387 | (1) |
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25-14 Vaginal Langerhans cells capture and internalize HIV-1 |
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387 | (1) |
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25-15 Vaginal CD4+ T cells bind, take up, and support HIV-1 replication |
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388 | (1) |
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25-16 Cervico-vaginal dendritic cells (DCs) capture, disseminate, and trans infect mononuclear cells |
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388 | (1) |
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25-17 Cell-associated HIV-1 is transmitted across inner foreskin mucosa |
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388 | (1) |
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25-18 HIV-1 entry into gut mucosa is mediated by epithelial cells and DCs |
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389 | (1) |
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25-19 Few HIV-1 virions are transmitted in acute HIV-1 infection |
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390 | (1) |
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T-cell depletion in early HIV-1 infection |
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391 | (1) |
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25-20 HIV-1 causes rapid, profound, and prolonged CD4+ T-cell depletion in the intestinal mucosa |
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391 | (1) |
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25-21 HIV-1 alters intestinal epithelial permeability, promoting microbial translocation |
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392 | (2) |
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Mucosal infections associated with HIV-1 infection |
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393 | (1) |
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25-22 HIV-1-induced immunosuppression leads to opportunistic infection of gut mucosa by viral, parasitic, bacterial, and fungal pathogens |
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394 | (3) |
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395 | (1) |
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395 | (2) |
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Chapter 26 Infection-Driven Periodontal Disease |
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397 | (16) |
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Etiology of periodontal disease |
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398 | (1) |
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26-1 Biofilms are important for the development of periodontitis |
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398 | (1) |
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Bacterial-host mucosal interactions in periodontal disease |
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399 | (1) |
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26-2 PAMPs are important in periodontal disease |
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399 | (2) |
|
Acquired immunity and the chronic lesion |
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401 | (1) |
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26-3 T cell and B cell immune responses are involved in periodontitis |
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401 | (1) |
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26-4 Cytokines are involved in bone resorption in periodontitis |
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|
402 | (1) |
|
Inflammation drives the pathogenesis of periodontitis |
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403 | (1) |
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26-5 The arachidonic acid pathway is important in periodontal disease |
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403 | (1) |
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26-6 Regulation of inflammation is a major determinant of bacterial colonization and disease |
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|
404 | (1) |
|
26-7 Endogenous generation of pro-resolution agonists is important in periodontal disease |
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|
404 | (2) |
|
26-8 The resolution phase of acute inflammation is as important as the onset phase |
|
|
406 | (1) |
|
Endogenous resolving molecules as therapeutic agents in periodontal disease |
|
|
407 | (1) |
|
26-9 Resolvins can help prevent periodontitis |
|
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407 | (1) |
|
26-10 Resolvins can treat periodontitis |
|
|
408 | (5) |
|
Biofilms and inflammatory periodontitis |
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410 | (1) |
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410 | (1) |
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411 | (2) |
|
Chapter 27 Principles of Mucosal Vaccine Strategies |
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413 | (17) |
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Principles of mucosal vaccination |
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413 | (3) |
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27-1 The problem with mucosal vaccines is tolerance |
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416 | (1) |
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27-2 There are unique compartmentalization and cell-migration pathways in mucosal immune responses |
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417 | (2) |
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27-3 There is preferential dissemination of mucosal immune responses after different routes of vaccination |
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419 | (2) |
|
Mucosal vaccine formulations and delivery systems |
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|
420 | (1) |
|
27-4 The ability to divide, present native antigens, and stimulate innate immunity are key features of live attenuated vaccines |
|
|
421 | (1) |
|
27-5 Inactivated whole-cell bacterial oral vaccines are effective |
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|
421 | (1) |
|
27-6 Plant-based `edible' vaccines may represent a strategy for mucosal vaccination |
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|
422 | (1) |
|
27-7 Targeted mucosal vaccines can use lectins and microparticles |
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423 | (2) |
|
Limitations of mucosal vaccines due to unique conditions in the tropics and the age of the vaccinees |
|
|
423 | (1) |
|
Mucosal adjuvants and their function |
|
|
424 | (1) |
|
27-8 The ADP-ribosylating toxins and their derivatives are mucosal adjuvants |
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|
425 | (1) |
|
27-9 Autoimmune disease can be treated by mucosal vaccination |
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426 | (4) |
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427 | (1) |
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428 | (2) |
|
PART VII SPECIFIC IMMUNE-MEDIATED DISEASES OF MUCOSAL SURFACES |
|
|
430 | (73) |
|
Chapter 28 Celiac Disease |
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431 | (14) |
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431 | (1) |
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28-1 Villous blunting and crypt cell hyperplasia are characteristic histological features |
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431 | (1) |
|
28-2 Intraepithelial lymphocytes are prominent |
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432 | (1) |
|
28-3 Immune cells infiltrate the lamina propria |
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433 | (1) |
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434 | (1) |
|
28-4 HLA genes are associated with celiac disease |
|
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434 | (1) |
|
28-5 Non-HLA genes also contribute to celiac disease predisposition |
|
|
435 | (2) |
|
Adaptive immune response to gluten in celiac disease |
|
|
436 | (1) |
|
28-6 Gluten-reactive CD4+ T cells in the intestinal mucosa recognize specific gluten residues |
|
|
437 | (1) |
|
28-7 Tissue transglutaminase is involved in celiac disease pathogenesis |
|
|
438 | (1) |
|
28-8 Autoantibodies are present in celiac disease |
|
|
439 | (1) |
|
28-9 Oral antigen induces an inflammatory response |
|
|
439 | (1) |
|
Innate immunity and the stress response to gluten |
|
|
440 | (1) |
|
28-10 Innate immune cell responses may be induced by gluten |
|
|
440 | (1) |
|
28-11 Intraepithelial cytotoxic T lymphocytes with NK cell receptors, epithelial cells with nonclassical MHC class I molecules, and IL-15 contribute to disease pathogenesis |
|
|
440 | (2) |
|
Immunological tests in the diagnostic workup of celiac disease |
|
|
441 | (1) |
|
28-12 Antibodies to tissue transglutaminase and gluten are used to diagnose celiac disease |
|
|
442 | (1) |
|
28-13 Other tests have a complementary role in the diagnosis of celiac disease |
|
|
442 | (1) |
|
28-14 Immune-based therapy may have a future in celiac disease |
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442 | (3) |
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443 | (1) |
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444 | (1) |
|
Chapter 29 IgA Nephropathy |
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|
445 | (10) |
|
Clinical presentation of IgA nephropathy |
|
|
445 | (1) |
|
29-1 IgA nephropathy is characterized by sporadic and familial forms |
|
|
445 | (1) |
|
29-2 Definitive diagnosis of IgA nephropathy requires a renal biopsy |
|
|
446 | (1) |
|
29-3 IgA nephropathy is characterized by mesangial deposits of IgA |
|
|
446 | (1) |
|
The immunopathogenesis of IgA nephropathy |
|
|
446 | (1) |
|
29-4 IgA, the target of IgA immune complexes, is the major immunoglobulin isotype produced in the body |
|
|
447 | (1) |
|
29-5 Human IgA1 has a unique hinge region containing sites that are amenable to O-linked glycosylation |
|
|
447 | (2) |
|
29-6 Circulating IgA1 in IgA nephropathy contains aberrant O-linked glycans |
|
|
449 | (1) |
|
29-7 Anti-glycan antibodies develop against aberrantly glycosylated IgA1 in IgA nephropathy and form immune complexes |
|
|
449 | (1) |
|
29-8 Gal-deficient IgA1-containing immune complexes in IgA nephropathy are inflammatory |
|
|
450 | (1) |
|
29-9 Urinary immunoglobulins are potential biomarkers of IgA nephropathy |
|
|
451 | (4) |
|
|
|
453 | (1) |
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|
|
453 | (2) |
|
Chapter 30 Mucosal Manifestations of Immunodeficiencies |
|
|
455 | (18) |
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|
|
456 | (1) |
|
30-1 Congenital agammaglobulinemia, or X-linked agammaglobulinemia, is the prototypic disorder of genetically determined antibody deficiency |
|
|
456 | (1) |
|
30-2 Common variable immunodeficiency (CVID) is the most common form of clinically significant primary immunodeficiency |
|
|
457 | (3) |
|
30-3 IgA deficiency is the most common primary immunodeficiency |
|
|
460 | (1) |
|
Combined immunodeficiencies |
|
|
460 | (1) |
|
30-4 Severe combined immunodeficiencies (SCIDs) are a heterogeneous group of genetically determined disorders |
|
|
461 | (2) |
|
30-5 CD40 ligand (CD40L) deficiency is a disorder with broad immunologic consequences due to the wide range of cell types that express its receptor, CD40 |
|
|
463 | (1) |
|
30-6 CD40 deficiency is a disorder that reproduces the clinical phenotype of CD40L deficiency |
|
|
464 | (1) |
|
30-7 Major histocompatibility complex class II (MHC-II) deficiency leads to extensive deficiencies in humoral and cellular adaptive immune function |
|
|
464 | (1) |
|
30-8 Deficiency of a nuclear protein, SP110, of unknown function leads to hepatic veno-occlusive disease with immunodeficiency |
|
|
465 | (1) |
|
Immunodeficiencies affecting regulatory factors and populations of lymphocytes that produce these factors |
|
|
465 | (1) |
|
30-9 Genetically mediated Foxp3 deficiency leads to the immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome |
|
|
466 | (1) |
|
30-10 Wiskott-Aldrich syndrome (WAS), due to deficiency in Wiskott-Aldrich protein (WASp), affects multiple lineages of hematopoietic cells and consequently diverse aspects of immune function |
|
|
466 | (1) |
|
30-11 Deficiency of the IL-2Rα (CD25) chain has major effects on Treg function |
|
|
467 | (1) |
|
30-12 Genetically determined deficiency in the IL-10 receptor and IL-10 presents prominently with features associated with aberrant mucosal homeostasis |
|
|
467 | (1) |
|
Immunodeficiencies affecting primarily innate immune cells |
|
|
468 | (1) |
|
30-13 Chronic granulomatous disease is the archetypal example of a genetically specified disorder of phagocyte function |
|
|
468 | (2) |
|
30-14 NEMO (NFκB essential modulator) deficiency, or X-linked immunodeficiency with ectodermal dystrophy, is a disorder that typifies the consequences of innate defects which affect the epithelial barrier |
|
|
470 | (3) |
|
|
|
471 | (1) |
|
|
|
471 | (2) |
|
Chapter 31 Inflammatory Bowel Disease |
|
|
473 | (16) |
|
|
|
474 | (1) |
|
31-1 Epidemiological observations support the idea of a genetic basis of IBD |
|
|
474 | (1) |
|
31-2 IBD susceptibility genes were identified before the era of genome-wide association studies |
|
|
475 | (1) |
|
31-3 Genome-wide association studies reveal large numbers of genes associated with IBD |
|
|
476 | (1) |
|
31-4 Environmental factors are clearly involved in IBD pathogenesis |
|
|
477 | (1) |
|
31-5 Bacteria and potentially viruses are major drivers of pathogenic inflammation in the gut |
|
|
478 | (1) |
|
Association of IBD with innate immunity abnormalities |
|
|
479 | (1) |
|
31-6 Genes involved in innate immunity, endoplasmic reticulum stress, and autophagy are important in IBD |
|
|
479 | (1) |
|
31-7 Autophagy-related proteins are linked to IBD |
|
|
479 | (1) |
|
31-8 Impairment of intestinal epithelial cell function may also be a key factor for the development and/or perpetuation of colitis |
|
|
480 | (1) |
|
31-9 Excessive innate immune response toward the microbiota causes chronic inflammation in the gut |
|
|
481 | (1) |
|
31-10 Innate immunity dysfunction is linked to Crohn's disease and Crohn's-like disease |
|
|
482 | (1) |
|
31-11 NOD2/CARD15 is involved in the control of defensins in the gut |
|
|
483 | (1) |
|
Adaptive immunity in the pathogenesis of IBD |
|
|
484 | (1) |
|
31-12 Genes associated with T-cell activation and differentiation are also involved in IBD |
|
|
484 | (1) |
|
31-13 Ongoing inflammation in IBD is driven by T cells |
|
|
484 | (5) |
|
|
|
487 | (1) |
|
|
|
487 | (2) |
|
Chapter 32 Food Sensitive and Eosinophilic Enteropathies |
|
|
489 | (14) |
|
Basic principles of the immune response to foods |
|
|
489 | (1) |
|
32-1 Healthy individuals are tolerant to the great diversity of antigens present in food |
|
|
489 | (1) |
|
32-2 Aberrant immune responses to foods can be IgE and non-IgE mediated |
|
|
490 | (1) |
|
32-3 Food sensitive enteropathies are diagnosed by laboratory and clinical parameters |
|
|
491 | (1) |
|
32-4 Induction of food-specific IgE can lead to mast-cell degranulation and both local and systemic allergic symptoms |
|
|
492 | (1) |
|
32-5 Eight types of food account for most allergic responses |
|
|
493 | (1) |
|
32-6 Allergies initially manifest at peripheral sites such as the skin, but progress to the airways |
|
|
494 | (1) |
|
32-7 Sensitization to food antigens may occur outside the gastrointestinal tract |
|
|
495 | (1) |
|
32-8 Food allergy has a genetic component |
|
|
495 | (1) |
|
32-9 The best time to introduce food antigens into the infant diet is unclear |
|
|
495 | (1) |
|
The eosinophilic gastrointestinal diseases (EGIDs) |
|
|
496 | (1) |
|
32-10 The definitions of mucosal eosinophilia are confusing |
|
|
496 | (1) |
|
32-11 Eosinophilic esophagitis (EoE) is the most common form of EGID |
|
|
497 | (1) |
|
32-12 The environmental allergens that contribute to EoE are dietary and airborne |
|
|
497 | (1) |
|
32-13 Eosinophils play a critical role in the pathogenesis of EoE |
|
|
497 | (1) |
|
32-14 Eosinophilic gastroenteritis is uncommon |
|
|
498 | (1) |
|
32-15 Allergic reactions to foods sometimes manifest only in the colon |
|
|
498 | (5) |
|
Prevalence of food sensitive enteropathies |
|
|
499 | (1) |
|
Treatment for food sensitive enteropathies |
|
|
499 | (1) |
|
|
|
500 | (1) |
|
|
|
501 | (2) |
| Index |
|
503 | |
