Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System

Wendy S. Garrett, Graham M. Lord, Shivesh Punit, Geanncarlo Lugo-villarino, Sarkis k. Mazmanian, Susumu Ito, Jonathan N. Glickman, Laurie H. Glimcher

Research output: Contribution to journalArticlepeer-review


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.
Original languageEnglish
Pages (from-to)33-45
Issue number1
Publication statusPublished - 4 Oct 2007


  • cellimmuno
  • humdisease
  • microbio


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