A study of the innovative treatment for rheumatoid arthritis by regulating signal crosstalk via DcR3
| Project/Area Number |
15K10473
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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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| Research Field |
Orthopaedic surgery
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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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| Research Collaborator |
FUKUDA Koji
MAEDA Toshihisa
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 関節リウマチ / リウマチ滑膜線維芽細胞 / 滑膜線維芽細胞 |
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| Outline of Final Research Achievements |
We newly found and reported that the expression of IL-12B(p40) was up-regulated by DcR3 specifically in rheumatoid fibloblast-like synovial fibroblasts (RA-FLS) in Molecular Medicine Reports. We also reported that Decoy receptor 3 down-regulates centrosomal protein 70kDa specifically in rheumatoid synovial fibroblasts in Modern Rheumatology. Further, we reported the expression profiling of genes in RA-FLS regulated by tumor necrosis factor-like ligand 1A in Biomedical Reports. Consequently, DcR3-TL1A signaling on RA synovial fibroblasts is shown as a possible new treatment target of RA.
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| Academic Significance and Societal Importance of the Research Achievements |
TNFデコイ受容体であるDcR3により関節リウマチ(RA)滑膜線維芽細胞(FLS)において発現が制御される遺伝子のうち、IL-12B(p40)とCEP70がDcR3-TL1Aシグナル系におけるRA治療標的分子であること、ならびに、DcR3のリガンドであるTL1AによりRA-FLSにおいて発現が制御される一連の遺伝子を解明したことは、RAの新しい治療標的分子を明らかにした点で高い意義を有する。
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Report
(5 results)
Research Products
(18 results)
