| Project/Area Number |
22390201
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Kyoto University |
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Principal Investigator |
MIMORI Tsuneyo 京都大学, 大学院・医学研究科, 教授 (10157589)
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| Co-Investigator(Renkei-kenkyūsha) |
FUJII Takao 京都大学, 大学院・医学研究科, 准教授 (70255462)
USUI Takashi 京都大学, 大学院・医学研究科, 非常勤講師 (90362483)
OHMURA Koichiro 京都大学, 大学院・医学研究科, 講師 (40432372)
NOJIMA Takaki 京都大学, 大学院・医学研究科, 非常勤講師 (30327514)
TANAKA Masao 金沢医科大学, 医学部, 准教授 (10332719)
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| Research Collaborator |
IGUCHI Mikiko 京都大学, 大学院・医学研究科, 研究生
MURAKLAMI Kosaku 大阪赤十字病院, 医師
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2012: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2011: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2010: ¥8,060,000 (Direct Cost: ¥6,200,000、Indirect Cost: ¥1,860,000)
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| Keywords | カルパイン / カルパスタチン / FRP / Th17 細胞 / 自己抗体 / 関節リウマチ / 自己免疫疾患 / フォリスタチン関連蛋白 / 炎症性ｻｲﾄｶｲﾝ / T細胞分化 / サイトカイン / 破骨細胞 |
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| Research Abstract |
We reported previously that autoantibodies to calpastatin (inhibitor of calpain (calcium-dependent neutral proteinase)) and follistatin-related protein (FRP) are found in patients with rheumatoid arthritis. Since these target antigens appeared to show regulatory effects against inflammation, we have intended to clarify the possibility that arthritis may be treated by regulating these autoantigens and autoantibodies. Calpastatin inhibited not only the secretion of IL -6 from fibroblasts, but also affected T cell differentiation, in particular strongly suppress ed the differentiation and activation of Th17 cell. Although FRP has been debated to show different action on regulating of inflammation between human and mouse, we demonstrated that FRP activates inflammation in natural immunity system via TLR4 -CD14 signaling. Analyses of these inflammation-regulating proteins may clarify the pathogenic mechanisms and novel therapeutic strategies of inflammatory arthritis and autoimmune diseases
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