| First Author | Garrett WS | Year | 2007 |
| Journal | Cell | Volume | 131 |
| Issue | 1 | Pages | 33-45 |
| PubMed ID | 17923086 | Mgi Jnum | J:141481 |
| Mgi Id | MGI:3818379 | Doi | 10.1016/j.cell.2007.08.017 |
| Citation | Garrett WS, et al. (2007) Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. Cell 131(1):33-45 |
| abstractText | Inflammatory bowel disease (IBD) has been attributed to overexuberant host immunity or the emergence of harmful intestinal flora. The transcription factor T-bet orchestrates inflammatory genetic programs in both adaptive and innate immunity. We describe a profound and unexpected function for T-bet in influencing the behavior of host inflammatory activity and commensal bacteria. T-bet deficiency in the innate immune system results in spontaneous and communicable ulcerative colitis in the absence of adaptive immunity and increased susceptibility to colitis in immunologically intact hosts. T-bet controls the response of the mucosal immune system to commensal bacteria by regulating TNF-alpha production in colonic dendritic cells, critical for colonic epithelial barrier maintenance. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new perspectives on the pathophysiology of IBD. |
