| Project/Area Number |
15K19667
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Research Collaborator |
MURAMATSU KEN 北海道大学, 大学院医学研究科, 大学院生
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 水疱性類天疱瘡 / 自己免疫疾患 / 制御性T細胞 / Scurfyマウス / 疾患モデル動物 / IPEX症候群 / BP230 / 17型コラーゲン / ノックアウトマウス |
|---|
| Outline of Final Research Achievements |
Regulatory T cells (Treg) are a T cell subset which play an important role on the self-tolerance. The master transcription factor of Treg is Foxp3, and its gene mutations induce severe systemic autoimmunity in mice (scurfy mice) and humans (IPEX syndrome). This study demonstrates that the absence of Tregs induce autoantibodies to epidermal basement membrane zone. We further revealed that the autoantibodies in scurfy mice and IPEX patients target bullous pemphigoid antigens, BP230 and type XVII collagen. These results suggest that a dysfunction of Tregs may trigger the development of bullous pemphigoid.
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