2012 Fiscal Year Final Research Report
Mechanism of bone and cartilage deterioration in rheumatoid arthritis via RANKL/Fas signaling
| 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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| Keywords | 歯科矯正学 |
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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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[Journal Article] Fas-independent T-cell apoptosis by dendritic cells controls autoimmune arthritis in MRL/lprmice2012
Author(s)
Izawa T, Kondo T, Kurosawa M, Oura R, Matsumoto K, Tanaka E, Yamada A, Arakaki R, Kudo Y, Hayashi Y, Ishimaru N
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Journal Title
PLoS One
Volume: Vol.7, No.12
Pages: e48798.
DOI
Peer Reviewed
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