| Project/Area Number |
23591439
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 | Nagasaki University |
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Principal Investigator |
KAWAKAMI Atsushi 長崎大学, 医歯(薬)学総合研究科, 教授 (90325639)
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| Co-Investigator(Kenkyū-buntansha) |
ORIGUCHI Tomoki 長崎大学, 大学院医歯薬学総合研究科, 教授 (90295105)
ABIRU Norio 長崎大学, 大学院医歯薬学総合研究科, 准教授 (00380981)
OHYAMA Kaname 長崎大学, 大学院医歯薬学総合研究科, 准教授 (50437860)
TAMAI Mami 長崎大学, 大学院医歯薬学総合研究科, 講師 (60380862)
ARIMA Kazuhiko 長崎大学, 大学院医歯薬学総合研究科, 講師 (30423635)
YAMASAKI Satoshi 広島大学, 大学病院, 助教 (30367388)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | リウマチ学 / RA / 滑膜細胞 / TSP-1 / TGF-β1 / VEGF / サイトカイン／増殖因子 / 疾患活動性 / パワードプラ / サイトカイン/増殖因子 / seronegative RA / イムノコンプレキソーム / LC-MS/MS / PF-4 / FLS / サイトカイン・増殖因子 |
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| Research Abstract |
Serum immune complexome analysis has found that TSP-1 and PF-4 are candidate autoantigens in RA. Especially, TSP-1 was considered as more useful than PF-4 in terms of detection sensitivity. In fact, prominent expression of TSP-1 was found in RA synovial tissues. TSP-1 was spontaneously produced in RA synovial cells and TGF- beta1 significantly stimulated the synthesis of TSP-1 at transcriptional level. A clear reduction of plasma TSP-1 and TGF- beta1 was found in RA patients successfully treated by disease-modifying anti-rheumatic drugs (DMARDs), however, the above change was not determined in RA patients DMARDs did not improve the clinical disease activity. It has been reported that the inflammatory niche of rheumatoid synovial tissues contain high TGF- beta1. We suspect that TGF- beta1 acts on synovial cells to produce TSP-1, and furthermore, the augmented production of TSP-1 may stimulate the autoantibody production toward TSP-1 in patients with RA.
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