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108 reviewsDysfunctional NF-κB signaling is critically involved in inflammatory boweldisease (IBD). We investigated the mechanism by which RIPK1 and TRADD, twokey mediators of NF-κB signaling, in mediating intestinal pathology using TAK1IEC deficient model. We show that phosphorylation of TRADD by TAK1 modulates RIPK1-dependent apoptosis. TRADD and RIPK1 act cooperatively tomediate cell death regulated by TNF and TLR signaling. We demonstrate thepathological evolution from RIPK1-dependent ileitis to RIPK1- and TRADD-codependent colitis in TAK1 IEC deficient condition. Combined RIPK1 inhibitionand TRADD knockout completely protect against intestinal pathology andlethality in TAK1 IEC KO mice. Furthermore, we identify distinctive microbiotadysbiosis biomarkers for RIPK1-dependent ileitis and TRADD-dependent colitis. These findings reveal the cooperation between RIPK1 and TRADD inmediating cell death and inflammation in IBD with NF-κB deficiency and suggest the possibility of combined inhibition of RIPK1 kinase and TRADD as a newtherapeutic strategy for IBD.
