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Mucosal Immunity

Lo-Intro to Mucosal Immunity

intestinal cellular turnover shed and turnover 2-5 days
mucosal type I single-layered epithelium
mucosal type II stratified epithelium
organized lymphoid tissue 1) tonsil 2) appendix 3) mesenteric lymph nodes 4) Peyer's patches 5) isolated lymphoid follicles 6) cryptopatches
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
isolated lymphoid follicles structurally similar to Peyer's patches-->characterized by single follicle
cryptopatches submucosal collections of lymphoid cells precursors to isolated lymphoid follicles
tonsil palatine and nasopharyngeal
appendix blind-ended tube connected to cecum
mesenteric lymph nodes lie in between layers of mesentery (double layer of peritoneum that suspends jejunum and ileum from posterior wall of abdomen)
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
TLR2 ligand binds gram (+) bacteria
TLR4 ligand binds LPS
TLR5 ligand binds bacterial flagellin
TLR9 ligand binds CpG
innate immunity early capability to recognize and degrade pathogens general response to PAMPs mediated by epithelial cells, TLRs, macrophages, mast cells, eosinophils, NK cells
adaptive immunity memory responses to previous exposure to pathogen very specific but delayed responses mediated by T and B lymphocytes
hygiene theory early and frequent exposure to infectious organisms boosts the immune system probiotic bacteria alter intestinal flora and immunity (and do not colonize)
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
Ulcerative Colitis IBD that usually presents with bloody diarrhea continuous distribution restricted to superficial epithelium of colon genetic association with HLA*DR2/DR3*QD2
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
Created by: kphom001