| Project/Area Number |
24659522
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SATO Shinichi 東京大学, 医学部附属病院, 教授 (20215792)
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| Co-Investigator(Kenkyū-buntansha) |
ASANO Yoshihide 東京大学, 医学部附属病院, 講師 (60313029)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 全身性強皮症 / トポイソメラーゼI / 完全フロイドアジュバンド / IL-6 / 皮膚硬化 / 肺線維化 / 自己免疫 / 免疫学 |
|---|
| Research Abstract |
To assess the contribution of anti-DNA topoisomerase I(anti-topo I)antibody, tissue fibrosis and cytokine production were examined in mice treated with topo I and either Freund's complete adjuvant (CFA) or Freund's incomplete adjuvant(IFA).
Treatment with topo I and CFA,in contrast to treatment with topo I and IFA,induced skin and lung fibrosis with increased interleukin (IL)-6 and IL-17 production. Anti-topo I antibody levels were greater in mice treated with topo I and CFA than with topo I and IFA.Furthermore,treatment with topo I and CFA increased Th2 and Th17 cell frequencies in bronchoalveolar lavage fluid,whereas treatment with topo I and IFA increased Th1 and Treg cell frequencies.Moreover,loss of IL-6 expression ameliorated skin and lung fibrosis and decreased Th2 and Th17 cell frequencies. This study shows that treatment with topo I and CFA induces SSc-like tissue fibrosis and autoimmunity.
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