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Abstract The regulatory mechanisms that maintain colonic immune homeostasis remain incompletely understood. Here we show that genetic deletion of Zbtb44, a previously uncharacterized member of the ZBTB transcription factor family, leads to spontaneous colitis and rectal prolapse. Zbtb44−/− T cells expressed increased IFN-γ, a pro-inflammatory cytokine strongly associated with human inflammatory bowel disease.
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