| Project/Area Number |
23659966
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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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 |
TANAKA Eiji 徳島大学, 大学院・へルスバイオサイエンス研究部, 教授 (40273693)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Shingo 徳島大学, 大学院・へルスバイオサイエンス研究部, 准教授 (40332796)
HIASA Masahiro 徳島大学, 大学院・へルスバイオサイエンス研究部, 助教 (90511337)
FUJIHARA Shinji 徳島大学, 病院, 助教 (70403706)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 歯科矯正学 / 関節リウマチ / RANKLシグナル / 破骨細胞 / 免疫細胞 / 関節骨破壊 / 樹状細胞 |
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| Research Abstract |
In this study, we investigated the functions of osteoclasts (Ocs) from MRL/lpr mice, animal model for human rheumatoid arthritis (RA), bearinf a mutant of Fas gene. In vitro and in vivo experiments showed enhanced function of MRL/lpr Ocs as antigen-presenting cells to activate peripheral T cells. Furthermore, the migratory response of MRL/lpr Ocs to S1P was significantly enhanced. The hyperfunctions of Ocs in MRL/lpr mice play a potent role in the pathogenesis for RA with bone destruction. Fas signaling of Ocs may regulate the differentiation, activation, and migration of Ocs.
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