| Project/Area Number |
25460825
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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 |
Hygiene and public health
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
Lee Suni 川崎医科大学, 医学部, 助教 (70414026)
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| Co-Investigator(Kenkyū-buntansha) |
Otsuki Takemi 川崎医科大学, 医学部, 教授 (40160551)
Nishimura Yasumitsu 川崎医科大学, 医学部, 准教授 (90360271)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 粉塵曝露 / 珪酸 / 自己免疫疾患 / 免疫動態 |
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| Outline of Final Research Achievements |
Silicosis patients frequently complicate with autoimmune diseases. Here, we analyzed the effect of silica particles on peripheral blood mononuclear cells (PBMC) in vitro and plasma factors to compare between silicosis patients (Sil) and healthy volunteers (HV). We found IL-6 and IL-23 were increased in culture media after silica particle exposure on PBMC from HV. Both cytokines are essential for polarization and maintain to Th17, critical T cell subset for autoimmune pathogenesis. Dysregulation of apoptosis has been considered to play a role in the pathogenesis of autoimmune diseases. DcR3 is known as an intrinsic decoy receptor inhibits FasL-induced apoptosis. Although plasma DcR3 and several major autoantibodies were increased in Sil, there are no correlation between DcR3 and the other clinical factors including autoantibodies.
Taken together, silica particles affect directly on PBMC to induce Th17 subset. Plasma DcR3 elevation in Sil indicates abnormal activation of immune system.
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