| Project/Area Number |
20790704
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
|---|
| Research Field |
膠原病・アレルギー・感染症内科学
|
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| Research Institution | University of Occupational and Environmental Health, Japan |
|---|
Principal Investigator |
NAKANO Kazuhisa University of Occupational and Environmental Health, Japan, 医学部, 助教 (50406500)
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|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
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| Keywords | 関節リウマチ / ドパミン / T細胞分化 / 樹状細胞 |
|---|
| Research Abstract |
We revealed that dendritic cells (DCs) were one of sources of dopamine in the synovial tissue of RA. During antigen-specific interaction with naive T-cells, dopamine released by DCs bound to D1-like dopamine receptors, induced differentiation to Th17 cells via IL-6 production. D2-like receptor-antagonists significantly induced accumulation of IL-6- and IL-17- positive T cells with remarkable angiogenesis, increased multiple layers of synovial fibroblast and exacerbated cartilage destruction in SCID-HuRAg mice, whereas antagonizing D1-like-receptor suppressed these responses.
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