2022 Fiscal Year Final Research Report
Analysis of CARD9 function in pulmonary mycobacterial infection
Project/Area Number |
20K16285
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 49070:Immunology-related
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Research Institution | Fukuoka Dental College (2021-2022) Osaka University (2020) |
Principal Investigator |
Toyonaga Kenji 福岡歯科大学, 口腔歯学部, 助教 (90791567)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 宿主防御 / 抗酸菌感染 / Th1応答 |
Outline of Final Research Achievements |
CARD9 is known to play an essential role in innate immune signaling via C-type lectin receptors. CARD9-deficient mice were shown to be highly susceptible to Mycobacterium tuberculosis. In CARD9-deficient mice, the antigen-specific T cell response after infection is comparable to that of wild-type (WT) mice, and it is thus considered that CARD9 deficiency affects innate immunity rather than acquired T cell responses during infection. However, the contribution of CARD9 to early mycobacterial infection is poorly understood. To clarify the role of CARD9 in the early stages of mycobacterial infection, CARD9-deficient mice were infected intratracheally with M. bovis BCG. We found that bacterial loads in the lungs were comparable between WT and CARD9-deficient mice 7 and 21 days after infection. These results suggest that CARD9 might not contribute to the elimination of bacteria in the early stages of pulmonary M. bovis BCG infection.
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Free Research Field |
免疫学
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Academic Significance and Societal Importance of the Research Achievements |
マウス感染モデルを用いた解析や、様々な疫学的知見から、CARD9を介した自然免疫活性化は、病原体感染に対する重要な宿主防御機構の一つと考えられ、CARD9経路を増強させることによって、病原体の排除を促す試みもいくつか行われている。このことから、本研究において見出した知見は、CARD9を介した免疫活性化機構の解明だけでなく、関連する感染性疾患の新規治療法開発にも繋がる可能性がある。
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