Role of Toll-like Receptors in Spontaneous Commensal-Dependent Colitis
作者： Ruslan Medzhitov , Seth Rakoff-Nahoum , Liming Hao
DOI: 10.1016/J.IMMUNI.2006.06.010
关键词:
摘要: Inflammatory bowel disease (IBD) is thought to result from a dysregulated interaction between the host immune system and its commensal microflora. Heterogeneity of susceptibility in humans rodents suggest that multiple mechanisms are responsible for etiology IBD. In particular, deficiencies anti-inflammatory immune-suppressive play an important role development However, it unknown how indigenous microflora stimulates this response regulated. To address these questions, we investigated Toll-like receptor (TLR) signaling spontaneous, commensal-dependent colitis interleukin (IL)-2- IL-10-deficient mice. We report was dependent on TLR Il10(-/-) contrast, Il2(-/-) mice developed intestinal inflammation absence pathways. These results demonstrate differential innate recognition by TLRs colitis.
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