| Project/Area Number |
23659703
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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 |
Orthopaedic surgery
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Norimasa 北海道大学, 大学院・医学研究科, 教授 (30322803)
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 関節リウマチ / 軟骨 / 骨 / Syndecan-4 |
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| Research Abstract |
In this study, to try to understand the role of Syndecan4 in the development of Rheumatoid Arthritis (RA), we have compared Syn4-deficient (Syn4 KO) mice and wild-type (WT) mice in collagen-induced arthritis (CIA) model. Syn4 KO mice revealed attenuated clinical severity and pathological features in CIA model. Syn4 was mainly expressed on B cells in the draining LN (dLN), and interestingly, Syn4 KO mice showed the drastic hypoplasia of germinal center formation in the dLN. And the numbers of B cell subsets that involve in germinal center formation in the dLN, were also decreased in Syn4 KO mice. In addition, Syn4 KO mice showed reduced production of type-II collagen-specific IgG antibodies (total IgG, IgG2a and IgG2b) compared with WT mice.Our results indicated that Syn4 on B cells possibly regulates the development of RA by modulating germinal center formation and antibody production.
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