| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
We focused on the function of the adaptor molecule CARD9, which is essential for NF-kB signaling pathway activation through ITAM-coupled receptors, and analyzed the role for innate immune activation through the CARD9 pathway in IFV infection. CARD9-deficient mice showed improved survival rate compared with control mice in pulmonary IFV infection. In CARD9-deficient mice, decrease in the production of inflammatory cytokines in BAL fluid and the inflammatory cell infiltration was observed, and the amount of viral RNA in the lungs was also slightly decreased compared with control mice. Cytokine production by macrophages stimulated with IFV remained unchanged, but that by bone marrow-derived conventional DCs or plasmacytoid DCs was decreased in CARD9-deficient mice. Collectively, our findings indicate that activation of innate immunity through the CARD9 pathway in DCs is involved in the excessive inflammation in IFV-infected lungs.
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