2021 Fiscal Year Final Research Report
Finding a new strategy for the treatment of interstitial pneumonia with Innate immunity system
Project/Area Number |
19K17668
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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 53030:Respiratory medicine-related
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Research Institution | The University of Tokyo |
Principal Investigator |
Ishii Takashi 東京大学, 保健・健康推進本部, 助教 (30803118)
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | 肺繊維症 / 間質性肺炎 / 自然免疫系 |
Outline of Final Research Achievements |
We investigated the role of MDA5, one of innate immune receptors that recognizes viral nuclear acid, in the pathogenesis of interstitial pneumonia/ lung fibrosis. Comparing the lung fibrosis model induced by bleomycin between wild-type and MDA5 deficient mice, we assume that MDA5 plays a protective role in the pathogenesis of lung fibrosis. We further demonstrated that MDA5 may regulate the activation of macrophages, the increase on lung neutrophils, and the function of Th17 cells which are involved in activity of neutrophils.
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Free Research Field |
呼吸器内科学
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Academic Significance and Societal Importance of the Research Achievements |
間質性肺炎/肺線維症は治療薬が十分になく、予後不良の疾患である。間質性肺炎の病態はマクロファージや好中球のような自然免疫系細胞が関わっており、肺胞上皮や線維芽細胞などの構造細胞との相互作用が考えられるが、その機序や自然免疫系との関わりはいずれも十分に解明されていない。今回ウイルス核酸を認識する自然免疫受容体MDA5に焦点を当て、MDA5の間質性肺炎における新しい役割の解明を行った事でMDA5の機能に基づいた間質性肺炎に対する新しい治療候補として今後発展しうると考えられる。
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