| Project/Area Number |
16H05323
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
Yamano Yoshihisa 聖マリアンナ医科大学, 医学研究科, 教授 (80445882)
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| Co-Investigator(Kenkyū-buntansha) |
山岸 誠 東京大学, 大学院新領域創成科学研究科, 特任講師 (90625261)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2018: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2016: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | 神経病態免疫学 / HAM / HTLV-1 / エピジェネティクス / エピゲノム操作 / ゲノム操作 |
|---|
| Outline of Final Research Achievements |
The main feature of Human T-cell leukemia virus type I (HTLV-1) -associated myelopathy (HAM) pathogenesis is a virus-induced hyperactive immune response that produces chronic inflammation in the central nervous system (CNS), but the mechanism by which HTLV-1 deregulates the immune response is unknown. We demonstrated that the overexpression of proinflammatory genes such as interferon-gamma, T-bet, C-X-C motif chemokine receptor 3 (CXCR3) were the key difference of HTLV-1 infected cells in patients with HAM compared to those in patients with adult T-cell leukemia/lymphoma (ATL) , a cancer caused by the same HTLV-1 virus that causes HAM. Furthermore, we found that the overexpression of histone methylation enzyme is involved in the acquisition and maintenance of those traits.
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| Academic Significance and Societal Importance of the Research Achievements |
近年、エピゲノム創薬は様々な疾患においても有望視されており、本研究で推進するHTLV-1関連脊髄症（HAM）の病態形成におけるエピゲノム異常の役割に関する解析は、HAMを起点として多くの難病への病態解明や新薬開発にも貴重な情報となり、将来の医療発展にも大きく寄与すると期待される。
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