| Project/Area Number |
23659500
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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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 |
USUI Takashi 京都大学, 医学研究科, 非常勤講師 (90362483)
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | IL-17 / マイクロアレイ / エピジェネティック制御 / ChiP 解析 / エピジェネティック / ChiP解析 / 炎症 / エピゲノム制御 |
|---|
| Research Abstract |
IL-17 is an important cytokine in the pathogenesis of autoimmune inflammatory disease, including collagen disease. We established stable murine T cell clones which produce a large amount of IL-17 as well as its low producer from the same T cell line. Then we can analyzed its molecular mechanisms by DNA sequence, RNA (microarray) and epigenetic levels. Although we could not differences in DNA sequence in the promoter region and the expressions of transcriptional factors, we found methylationand de-methylation status were quite different in these clones. Furthermore, we found gene-X could control it. These findings will lead to new-generation strategy for controlling autoimmune inflammatory disease, including collagen disease.
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