2013 Fiscal Year Final Research Report
Elucidation of innate immune responses through ITAM coupled receptor-CARD9 signaling in influenza virus infection.
Project/Area Number |
23790919
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Respiratory organ internal medicine
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Research Institution | Kitasato University |
Principal Investigator |
UEMATSU Takayuki 北里大学, 北里大学メディカルセンター, 上級研究員 (90414060)
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Project Period (FY) |
2011 – 2013
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Keywords | 自然免疫 / 肺炎 / インフルエンザウイルス |
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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Research Products
(11 results)