| Project/Area Number |
17K09776
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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 |
Neurology
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| Research Institution | Niigata University |
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Principal Investigator |
KAWACHI Izumi 新潟大学, 医歯学系, 准教授 (40432083)
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| Co-Investigator(Kenkyū-buntansha) |
豊島 靖子 新潟大学, 脳研究所, 准教授 (20334675)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 視神経脊髄炎 / 多発性硬化症 / アストロサイト / 自然免疫 / マクロファージ |
|---|
| Outline of Final Research Achievements |
Neuromyelitis optica (NMO) is an autoimmune CNS disorder, which is characterized by aquaporin-4 water channel (AQP4) autoantibodies. Based on our pathological study using autopsied samples from NMO cases, CNS lesions at initial/early active stages in NMO included some granulocytes, interleukin-17-producing T cells and macrophages. These data suggest that these cells might provide initial signals, which induce entry of AQP4 autoantibodies from the outside of CNS via blood-brain barrier, and contribute active CNS lesions in NMO.
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| Academic Significance and Societal Importance of the Research Achievements |
視神経脊髄炎はアクアポリン4自己抗体と補体が関連する中枢神経系自己免疫疾患であり, 本邦に多い指定難病の一つである. 早期病変にTH17/TC17をはじめとした新たな炎症向性リンパ球・顆粒球と炎症向性マクロファージ・ミクログリアを新たに見出した. 同細胞を抑制する分子標的治療の開発に向けた病態基盤の一部を確立したという点で意義があると考えられる.
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