| Project/Area Number |
18K09106
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 56020:Orthopedics-related
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| Research Institution | Kobe University |
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Principal Investigator |
Miura Yasushi 神戸大学, 保健学研究科, 准教授 (60346244)
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 関節リウマチ / リウマチ滑膜細胞 / リウマチ滑膜線維芽細胞 / デスレセプター / 滑膜線維芽細胞 / 滑膜細胞 |
|---|
| Outline of Final Research Achievements |
With the aim of elucidating the pathogenesis of rheumatoid arthritis characterized by chronic destructive polyarthritis, the human-specific TNF decoy receptor Decoy receptor3 (DcR3), which functions as a both decoy receptor and a ligand in three TNF/TNF receptor signaling pathways: TL1A and DR3, LIGHT and HVEM/BTLA, and FasL and FAS. We investigated the genes involved in the signal transduction of DcR3 in rheumatoid synovial cells. As a result, we identified genes and gene groups that can serve as targets for molecular targeted therapy related to apoptosis induction and proliferation suppression of rheumatoid arthritis synovial cells.
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| Academic Significance and Societal Importance of the Research Achievements |
TNFおとり受容体であるDcR3が関わる関節リウマチ滑膜細胞におけるシグナル伝達系において、発現が制御される遺伝子ならびに遺伝子群を新たに同定したことは、将来のRAの新しい治療標的開発に繋がる点で高い学術的ならびに社会的意義を有する。
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