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2018 Fiscal Year Final Research Report

IL-33R(+) cells and atopic dermatitis

Research Project

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Project/Area Number 17K16356
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Dermatology
Research InstitutionHyogo Medical University

Principal Investigator

NAGAI Makoto  兵庫医科大学, 医学部, 助教 (30791545)

Research Collaborator IMAI Yasutomo  
YASUDA Koubun  
Project Period (FY) 2017-04-01 – 2019-03-31
KeywordsILC2 / basophil
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.

Free Research Field

アトピー性皮膚炎

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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Published: 2020-03-30  

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