| Project/Area Number |
24659642
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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 |
Cerebral neurosurgery
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| Research Institution | Tohoku University |
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Principal Investigator |
FUJIMURA Miki 東北大学, 医学(系)研究科(研究院), 准教授 (00361098)
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| Co-Investigator(Kenkyū-buntansha) |
TOMINAGA Teiji 東北大学, 医学系研究科, 教授 (00217548)
FUJIMURA Taku 東北大学, 医学系研究科, 助教 (50396496)
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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 |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | moyamoya disease / immunity / regulatory T cell / Foxp3 / autoimmune response / etiology / autoimmune reponse |
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| Research Abstract |
Moyamoya disease is characterized by a progressive stenosis at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain. We investigated the role of regulatory T-cell (Treg) in the patho-physiology of moyamoya disease. Result showed that number of Foxp3-positive Treg was significantly lower in patients with moyamoya disease compared to normal control. We also compared the expression of Foxp3-positive Treg between mice lacking RNF213 (susceptibility gene for moyamoya disease) and wild-type mice, but there was no significant difference. These results suggested that autoimmune response mediated by Treg may play a role in the patho-physiology of moyamoya disease.
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