Analysis of the mechanism of erythema formation via IgE autoantibodies in bullous pemphigoid
| Project/Area Number |
17K16318
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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 |
IZUMI Kentaro 北海道大学, 医学研究院, 助教 (50793668)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 皮膚病態学 / 自己免疫 / 水疱症 / 水疱性類天疱瘡 / 基底膜タンパク / 免疫学 / 蛋白質 / 酵素 |
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| Outline of Final Research Achievements |
Bullous pemphigoid (BP) is clinically characterized by blisters and erythema with pruritis. We found that basophils were activated in the peripheral blood from BP patients. It was suggested that basophil activation was based on the binding of type XVII collagen and BP-IgE autoantibody. Although type XVII collagen express along the basement membrane zone of epidermis under the steady state, we found that type XVII collagen was also localized in the superficial dermis in the lesional skin from a part of BP patients.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究にて水疱性類天疱瘡（BP）の血中好塩基球の活性化が17型コラーゲン-IgE自己抗体の結合に基づいて生じた可能性が示唆された。好塩基球の活性化は脱顆粒に引き続いて起こるケミカル・メディエーターの放出を介して血管透過性の亢進や皮膚炎症を惹起することから、17型コラーゲンとBP-IgE自己抗体の抗原-抗体反応がBPの病態に関与している可能性が考えられた。未だ、ステロイドの全身投与が治療の第一選択であるBPにおいてBP-IgE自己抗体を介した好塩基球の活性化がBPの新規治療法に繋がる可能性が示唆された。
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Report
(4 results)
Research Products
(2 results)
