Journal
CELL
Volume 131, Issue 1, Pages 33-45Publisher
CELL PRESS
DOI: 10.1016/j.cell.2007.08.017
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Funding
- Medical Research Council [G108/380] Funding Source: researchfish
- Medical Research Council [G108/380] Funding Source: Medline
- NCI NIH HHS [R01 CA112663, R01 CA112663-07, CA112663, R01 CA112663-06] Funding Source: Medline
- NIAID NIH HHS [P01 AI056296-05, P01 AI056296, P01 AI056296-03, P01 AI056296-02, P01 AI056296-04, AI56296, P01 AI056296-010001, P01 AI056296-01] Funding Source: Medline
- MRC [G108/380] Funding Source: UKRI
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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.
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