| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
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.
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