Analysis of monocytes involved in joint destruction and joint repair in rheumatoid arthritis
Project/Area Number |
24591455
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
膠原病・アレルギー・感染症内科学
|
Research Institution | Tokyo Dental College (2014) Keio University (2012-2013) |
Principal Investigator |
SETA noriyuki 東京歯科大学, 歯学部, 准教授 (40338372)
|
Co-Investigator(Kenkyū-buntansha) |
KUWANA Masataka 慶應義塾大学, 医学部, 准教授 (50245479)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | 関節リウマチ / 末梢血単球 |
Outline of Final Research Achievements |
The number of circulating CD14+CD15-CXCR4high monocytes (Mos) possibly involved in joint repair in RA decreased in RA patients compared with that in healthy donors. Moreover, the expression of IL-6, TNF alpha, and CCR5 were high in CD14+CD15+CXCR4low Mos possibly involved in joint destruction in RA, and the expression of CX3CR1 was high in CD14+CD15-CXCR4high Mos, indicating that these cell groups may be controled by different factors. Furhtermore, the number of circulating CD14brightCD16- (classical) Mos decreased in RA patients compared with that in healthy donors, and classical Mos were decreased in RA patients with a response to methotrexate after treatment. These results indicate that classical Mos also may involve in the joint destruction.
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Report
(4 results)
Research Products
(7 results)