| Question | Answer |
| 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 |
