Development of strategy to treat immune and allergic diseases targeting molecules associated with NF-kB activation

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We characterized two deficient mice lacking TRAF2 or c-FLIP, both of which are critically involved in protection of cells from TNFα-induced apoptosis. TRAF2-deficient mice spontaneously developed severe hepatitis through enhanced apoptosis of the colonic epithelial cells and subsequent alterations of the commensal microbiota and upregulation of proinflammatory cytokines. To delete c-Flip gene, we injected poly I:C into interferon-inducible c-Flip-deficient (c-FlipF/F:Mx) mice. Upon poly I:C injection, c-FlipF/F:Mx mice developed severe hepatitis along with upregulation of IL-6, but not TNFα or IL-1β. Collectively, these results suggest that deletion of adaptor molecules associated with TNFα signalings promotes apoptosis along with inflammation.