Role of Toll-like receptors in spontaneous commensal-dependent colitis

被引:297
作者
Rakoff-Nahoum, Seth
Hao, Liming
Medzhitov, Ruslan
机构
[1] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 USA
[2] Yale Univ, Sch Med, Immunol Sect, New Haven, CT 06510 USA
[3] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA
关键词
D O I
10.1016/j.immuni.2006.06.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
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 disease susceptibility in humans and rodents suggest that multiple mechanisms are responsible for the etiology of IBD. In particular, deficiencies in anti-inflammatory and immune-suppressive mechanisms play an important role in the development of IBD. However, it is unknown how the indigenous microflora stimulates the immune system and how this response is regulated. To address these questions, we investigated the role of Toll-like receptor (TLR) signaling in the development of spontaneous, commensal-dependent colitis in interleukin (IL)-2- and IL-10-deficient mice. We report that colitis was dependent on TLR signaling in II10(-/-) mice. In contrast, II2(-/-) mice developed intestinal inflammation in the absence of TLR signaling pathways. These results demonstrate a differential role of innate immune recognition by TLRs in the development of commensal-dependent colitis.
引用
收藏
页码:319 / 329
页数:11
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