T-bet is a transcription factor that regulates immune responses in both adaptive and innate immunity. This study reveals an unexpected and critical role for T-bet in maintaining host-commensal relationships in the gut. T-bet deficiency in the innate immune system leads to spontaneous and communicable ulcerative colitis (UC) 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, which is critical for maintaining the colonic epithelial barrier. Loss of T-bet allows bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings highlight T-bet's role as a "peacekeeper" in host-commensal interactions and provide new insights into the pathophysiology of IBD. The study shows that T-bet deficiency in mice lacking an adaptive immune system results in severe, communicable colitis resembling human UC. This colitis is characterized by epithelial barrier breaches, increased TNF-α production in colonic dendritic cells, and the presence of colitogenic bacteria. T-bet regulates TNF-α production in colonic dendritic cells, which is essential for maintaining the integrity of the colonic epithelium. T-bet deficiency leads to increased TNF-α production, which drives tissue injury and colitis. T-bet also regulates the production of TNF-α in dendritic cells, which is critical for maintaining the balance between host immunity and autoimmunity. T-regulatory cells play a key role in controlling TRUC colitis. T-regulatory cells can suppress the development of colitis in T-bet-deficient hosts. The TRUC colitis model is highly transmissible, both vertically and horizontally, and is driven by the presence of colitogenic bacteria. The colitogenic bacteria can be transmitted to T-bet-sufficient hosts, leading to the development of colitis. The study also shows that T-bet deficiency in the innate immune system creates a niche for colitogenic bacteria, which can be transmitted to genetically intact hosts. The study provides a novel mouse model of spontaneous UC that offers exciting opportunities to further understand the etiology and pathogenesis of UC. It also highlights the importance of T-bet in maintaining host-commensal relationships and the role of T-regulatory cells in controlling colitis. The findings suggest that T-bet is not only a key regulator of type 1 immune responses but also a peacekeeper at the prokaryotic-eukaryotic interface. The study also highlights the importance of the gut microbiota in the development of IBD and the potential for targeting the microbiota as a therapeutic approach.T-bet is a transcription factor that regulates immune responses in both adaptive and innate immunity. This study reveals an unexpected and critical role for T-bet in maintaining host-commensal relationships in the gut. T-bet deficiency in the innate immune system leads to spontaneous and communicable ulcerative colitis (UC) 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, which is critical for maintaining the colonic epithelial barrier. Loss of T-bet allows bacterial populations to become colitogenic, and this colitis is communicable to genetically intact hosts. These findings highlight T-bet's role as a "peacekeeper" in host-commensal interactions and provide new insights into the pathophysiology of IBD. The study shows that T-bet deficiency in mice lacking an adaptive immune system results in severe, communicable colitis resembling human UC. This colitis is characterized by epithelial barrier breaches, increased TNF-α production in colonic dendritic cells, and the presence of colitogenic bacteria. T-bet regulates TNF-α production in colonic dendritic cells, which is essential for maintaining the integrity of the colonic epithelium. T-bet deficiency leads to increased TNF-α production, which drives tissue injury and colitis. T-bet also regulates the production of TNF-α in dendritic cells, which is critical for maintaining the balance between host immunity and autoimmunity. T-regulatory cells play a key role in controlling TRUC colitis. T-regulatory cells can suppress the development of colitis in T-bet-deficient hosts. The TRUC colitis model is highly transmissible, both vertically and horizontally, and is driven by the presence of colitogenic bacteria. The colitogenic bacteria can be transmitted to T-bet-sufficient hosts, leading to the development of colitis. The study also shows that T-bet deficiency in the innate immune system creates a niche for colitogenic bacteria, which can be transmitted to genetically intact hosts. The study provides a novel mouse model of spontaneous UC that offers exciting opportunities to further understand the etiology and pathogenesis of UC. It also highlights the importance of T-bet in maintaining host-commensal relationships and the role of T-regulatory cells in controlling colitis. The findings suggest that T-bet is not only a key regulator of type 1 immune responses but also a peacekeeper at the prokaryotic-eukaryotic interface. The study also highlights the importance of the gut microbiota in the development of IBD and the potential for targeting the microbiota as a therapeutic approach.