Critical Roles of TIPE2 Protein in Murine Experimental Colitis

摘要: Both commensal bacteria and infiltrating inflammatory cells play essential roles in the pathogenesis of bowel disease. The molecular mechanisms whereby these pathogenic factors are regulated during disease not fully understood. We report this article that a member TNF-α–induced protein 8 (TNFAIP8) family called TIPE2 (TNFAIP8-like 2) plays crucial role regulating dissemination cell function experimental colitis induced by dextran sodium sulfate (DSS). Following DSS treatment, TIPE2-deficient mice, or chimeric mice deficient only their hematopoietic cells, lost less body weight survived longer than wild-type controls. Consistent with clinical observation, exhibited significantly severe colonic damage. This was associated marked reduction expression cytokines, such as TNF-α, IL-6, IL-12. Importantly, ameliorated DSS-induced TIPE2−/− also reduced local weaker systemic response. Combined our previous is negative regulator antibacterial immunity, results indicate promotes inhibiting mucosal immunity to bacteria.