Cell
Volume 131, Issue 1, 5 October 2007, Pages 33-45
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Article
Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System

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Summary

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-α 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.

CELLIMMUNO
HUMDISEASE
MICROBIO

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Present address: Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, Natural Sciences Building 6104, La Jolla, CA 92093-0380, USA.

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These authors contributed equally to this work.