Study for the treatment of rheumatoid arthritis by regulating synovial proliferation with DcR3.
| Project/Area Number |
21591944
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kobe University |
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Principal Investigator |
MIURA Yasushi 神戸大学, 大学院・保健学研究科, 准教授 (60346244)
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| Research Collaborator |
立石 耕司
高橋 完靖
福田 康治
林 申也
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | リウマチ病学 / 関節リウマチ / デコイレセプター / アポトーシス / DcR3 / TL1A |
|---|
| Research Abstract |
We reported that decoy receptor 3(DcR3), a member of TNF receptor superfamily, inhibits Fas-induced apoptosis in THP-1 monocyte/macrophage cells and that DcR3 increases VLA4 adhesion molecule in THP-1 inhibiting cycloheximide-induced apoptosis. We also reported that serum DcR3 is elevated in patients with RA. Further, we reported that DcR3 inhibits the proliferation of RA synovial cells induced by inflammatory cytokines and the activation of MAPK by using TL1A expressing on the cell surface as a receptor. DcR3 is deeply involved in the pathogenesis of RA by not only as a decoy receptor against Fas ligand, but also as a ligand to inhibit apoptosis by increasing cell adhesion and to inhibit cytokine-induced cell proliferation. We revealed that DcR3 is a possible treatment target of RA.
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Report
(4 results)
Research Products
(23 results)
