| Project/Area Number |
21590448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IGARASHI Hideya 川崎医科大学, 医学部, 准教授 (40291538)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 疾患モデル動物 / 自己免疫疾患 / 関節リウマチ / サイトカイン / マウスモデル / ノックインマウス / IL-6 / gp130 / IL-17 |
|---|
| Research Abstract |
A model mouse for rheumatoid arthritis, gp130F759 exhibited increases of serum cytokines and autoantibodies, and infiltration of inflammatory cells in the synovium at 5-month-old, when the clinical arthritis is hardly detectable. Furthermore, increased tyrosine-phosphorylation of STAT3, as an aberrant gp130 signaling, and production of Padi4 protein that may involve in the autoantibody production, were detected in the joints. We found the earliest changes in the joints of gp130F759, which is informative for the understanding of the early pathophysiology of rheumatoid arthritis.
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