Regulation of bone and cartilage destruction via RANKL/Fassignaling crosstalk in temporomandibular joint.
| Project/Area Number |
20791579
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthodontic/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IZAWA Takashi The University of Tokushima, 大学院・ヘルスバイオサンエンス研究部, 助教 (30380017)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | RANKLシグナル / Fasシグナル / 樹状細胞 / 関節リウマチ / 関節骨・軟骨破壊 / アポトーシス / T細胞 / TRAILシグナル / RANKL / Fas / 破骨細胞 / MRL / lpr / Bcl-2 |
|---|
| Research Abstract |
The aim of this study was to analyze the effect of dedritic cells (DCs) transfer stimulated with RANKL on the development. of murine autoimmune arthropathy. Three times of RANKL-stimulated DCs transfer into arthritis model mice increased the T cell apoptosis in vivo, and protected the development of autoimmune arthritis. These data indicate that RANKL pathway plays a crucial role for immunomodulation of murine autoimmune arthropathy.
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Report
(3 results)
Research Products
(24 results)
