2009 Fiscal Year Final Research Report
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 |
Research Field |
Orthodontic/Pediatric dentistry
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Research Institution | The University of Tokushima |
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)
|
Project Period (FY) |
2008 – 2009
|
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 |
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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