Mechanisms of endothelial injury mediated by receptors of innate lymphocytes involved in vasculitis pathogenesis
| Project/Area Number |
18K15077
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49020:Human pathology-related
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| Research Institution | Shinshu University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 血管炎 / 内皮傷害 / 自然免疫 / 内皮細胞 / NKG2D / 自然免疫性リンパ球 |
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| Outline of Final Research Achievements |
The purpose of this study was to clarify how innate lymphocytes recognize the target (vascular endothelial cells) in endothelial cell injury by innate lymphocytes, which are thought to be involved in the pathogenesis of vasculitis, by co-culture experiments of innate lymphocytes cell line and endothelial cells.
When the NK cell line KHYG-1 (Effector cells) and endothelial cells (Target cells) were co-cultured, endothelial cells were observed to detach from the culture dish in an Effector/Target ratio dependent manner. However, no results were obtained to infer that the receptor NKG2D, which was a candidate as one of the target recognition mechanisms, was involved.
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| Academic Significance and Societal Importance of the Research Achievements |
血管炎・血管内皮細胞傷害は、敗血症などの致死性病態やCOVID-19などの重篤感染症における病態形成に関与していることから、このメカニズムの解明と血管内皮傷害を抑制することは治療法の開発につながることが期待される。本研究ではそのメカニズムについて自然免疫性リンパ球の受容体を介した内皮細胞傷害の関与を明らかにすることを目的としたが、受容体の候補の一つであったNKG2Dの関与は明らかにできなかった。
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Report
(5 results)
Research Products
(2 results)
