However, in the T cell transfer model of inflammatory bowel disease, we found accelerated and more severe colitis in Rag2−/− mice transferred CD4+CD45RBhi naive T cells lacking Trp73 compared to cells from WT littermates, together with the early and sustained development of pathogenic Th1 T cells in the colon tissues, consistent with the ability of Trp73 to restrain IFNγ production and Th1 development in a T cell-intrinsic manner. The gene discussed is CD4; the disease is inflammatory bowel disease.