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Lo-Intro to Mucosal Immunity

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Question
Answer
intestinal cellular turnover   shed and turnover 2-5 days  
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mucosal type I   single-layered epithelium  
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mucosal type II   stratified epithelium  
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organized lymphoid tissue   1) tonsil 2) appendix 3) mesenteric lymph nodes 4) Peyer's patches 5) isolated lymphoid follicles 6) cryptopatches  
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peyer's patches   most in small intestine and highest in terminal ileum 1:2 ratio of T-cells/B-cells pick up antigens thru M cells  
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isolated lymphoid follicles   structurally similar to Peyer's patches-->characterized by single follicle  
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cryptopatches   submucosal collections of lymphoid cells precursors to isolated lymphoid follicles  
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tonsil   palatine and nasopharyngeal  
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appendix   blind-ended tube connected to cecum  
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mesenteric lymph nodes   lie in between layers of mesentery (double layer of peritoneum that suspends jejunum and ileum from posterior wall of abdomen)  
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TLR expression and ligands   expressed by bone marrow-derived cells and tissue stroma ex) epithelium, fibroblasts ligands: 1) PAMPs 2) peptidoglycans 3) LPS 4) dsRNA 5) flagellin 6) CpG  
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TLR2 ligand   binds gram (+) bacteria  
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TLR4 ligand   binds LPS  
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TLR5 ligand   binds bacterial flagellin  
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TLR9 ligand   binds CpG  
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innate immunity   early capability to recognize and degrade pathogens general response to PAMPs mediated by epithelial cells, TLRs, macrophages, mast cells, eosinophils, NK cells  
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adaptive immunity   memory responses to previous exposure to pathogen very specific but delayed responses mediated by T and B lymphocytes  
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hygiene theory   early and frequent exposure to infectious organisms boosts the immune system probiotic bacteria alter intestinal flora and immunity (and do not colonize)  
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adaptive immune mechanisms   1) FAE-->exploited by pathogens bc of its uptake 2) oral tolerance-->lack of immune response to food 3) commensal bacteria 4) IgA  
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Ulcerative Colitis   IBD that usually presents with bloody diarrhea continuous distribution restricted to superficial epithelium of colon genetic association with HLA*DR2/DR3*QD2  
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Crohn's disease   IBD-usually presents with abdominal pain, intestinal obstruction, perforation chronic intermittent, transmural, segmental inflamm. c'some 16 (NOD2 gene)-->20x more susceptible-->reduced NF-kB activation ATG16L1 (autophagy) variants increases risk  
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