| Project/Area Number |
25870091
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
Immunology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
INOUE ASUKA 筑波大学, 医学医療系, 助教 (80636522)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 関節リウマチ / 炎症性サイトカイン / ケモカイン / 好中球 / 細胞遊走 / TIARP / マクロファージ / 滑膜細胞 / サイトカイン |
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| Outline of Final Research Achievements |
Recently, We found that TIARP functions as a negative regulator in autoimmune arthritis, although the molecular mechanism of TIARP-expressing cells in arthritis remains uncertain. The purpose of this study is to elucidate the functional role of TIARP in the pathogenesis of arthritis. The severity of arthritis in TIARP-/- mice was markedly exacerbated, and the recruitment of neutrophil into the joint was significantly enhanced. CXCR1/2 expression was significantly higher in TIARP-/- neutrophil, and the recruitment capacity was enhanced to the ligand of CXCL2. Serum-transferred arthritis in TIARP-/- mice was attenuated by the blockade of IL-6R signaling, and recruitment of neutriphil into the joint of TIARP-/- mice was suppressed. These results suggested that TIARP might down-regulate the production of CXCL2 and the expression of CXCR1/2, resulting in the protective ability of neutrophil migration in arthritic joints, probably via the inhibition of IL-6 signaling.
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