2014 Fiscal Year Final Research Report
Identification of cells responsible for osteoclastogenesis in arthritis
Project/Area Number |
25670636
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Orthopaedic surgery
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Research Institution | The University of Tokyo |
Principal Investigator |
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Project Period (FY) |
2013-04-01 – 2015-03-31
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Keywords | 破骨細胞 |
Outline of Final Research Achievements |
In order to functionally demonstrate in vivo which cell types drive pathogenic osteoclast differentiation we used Tnfsf11a floxed mice for the depletion of RANKL in T-cells and synovial fibroblasts during collagen antibody-induced arthritis (CAIA). The accurate assessment of the osteoclast erosions was performed by micro-CT analysis. Significant increases in osteoclast numbers and bone erosions were observed in the Tnfsf11flox/Δ Lck-Cre and Tnfsf11flox/Δ Col2a1-Cre groups during CAIA, however, the Tnfsf11flox/Δ Col6a1-Cre mice showed significant protection against osteoclast formation and bone erosions. Thus, it is suggested that RANKL expression by synovial fibroblasts rather than T-cells govern the osteoclast differentiation that leads to inflammation-associated joint destruction.
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Free Research Field |
骨免疫学
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