| Project/Area Number |
17K16356
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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 | Hyogo Medical University |
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Principal Investigator |
NAGAI Makoto 兵庫医科大学, 医学部, 助教 (30791545)
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| Research Collaborator |
IMAI Yasutomo
YASUDA Koubun
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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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 | ILC2 / basophil / IL-33 / 好塩基球 / アトピー性皮膚炎 |
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| Outline of Final Research Achievements |
IL-33 is an alarmin that promotes type 2 cytokine production, and a genetically modified mouse (IL-33Tg) that overproduces IL-33 is a model that reproduces the symptoms of atopic dermatitis (AD). In this study, we demonstrated that dermatitis of IL-33Tg is attenuated when basophils are eliminated, or when type 2 innate lymphoid cells (ILC2) are deleted. Thus, we revealed the cells targeted by IL-33.
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| Academic Significance and Societal Importance of the Research Achievements |
ヒトADでは好塩基球が皮膚で増加していることが近年報告された(Kim BS, J Immunol. 193(7):3717-25, 2014)が、ADの皮膚炎が好塩基球の活性化に依存するかどうか、実際にヒトで検討するのは難しい。そこで、我々の研究チームは、AD様皮膚炎を自然発症するIL-33Tgマウスを好塩基球のないマウスと交配あるいは抗体投与によって好塩基球を除去し、皮膚炎が減弱するという効果を観察したことで、ADの皮膚炎発症における好塩基球の役割が明らかとなった。
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