The study investigates the role of the transcription factor T-bet in maintaining host-commensal relationships in the gastrointestinal tract. T-bet deficiency in the innate immune system leads to spontaneous and communicable ulcerative colitis in the absence of adaptive immunity, and increases 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, which is critical for maintaining the integrity of the colonic epithelial barrier. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. The findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new insights into the pathophysiology of inflammatory bowel disease (IBD).The study investigates the role of the transcription factor T-bet in maintaining host-commensal relationships in the gastrointestinal tract. T-bet deficiency in the innate immune system leads to spontaneous and communicable ulcerative colitis in the absence of adaptive immunity, and increases 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, which is critical for maintaining the integrity of the colonic epithelial barrier. Loss of T-bet influences bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. The findings reveal a novel function for T-bet as a peacekeeper of host-commensal relationships and provide new insights into the pathophysiology of inflammatory bowel disease (IBD).