Regulatory mechanism of IL-33 in atopic dermatitis

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K08653
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53050:Dermatology-related
• Research Institution: Kyushu University
• Principal Investigator: Tsuji Gaku 九州大学, 大学病院, 准教授 (20423551)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: アトピー性皮膚炎 / IL-33 / IL-37 / 芳香族炭化水素受容体

Outline of Final Research Achievements

The pathogenesis of atopic dermatitis consists of skin barrier dysfunction, type 2 immune response, and pruritis. Keratinocyte-derived IL-33 is closely related to these factors. In this study, we investigated the mechanism of IL-33 production in human keratinocytes. In the first year, we found that the chemical sensor aryl hydrocarbon receptor regulates IL-33 production. In the second year, we found that IL-37, an anti-inflammatory cytokine, negatively regulates IL-33 expression. Finally, we showed that IL-37 was regulated by aryl hydrocarbon receptors and suggested a possibility that aryl hydrocarbon receptor regulates the pathogenesis of atopic dermatitis via the balance between IL-33 and IL-37.

Free Research Field

皮膚科学

Academic Significance and Societal Importance of the Research Achievements

本研究で用いたタピナロフという薬剤は、現在、アトピー性皮膚炎の新規薬剤としてPhase３試験が国内で施行中である。本研究によって、タピナロフがアトピー性皮膚炎に対してどのような機序で効果を発揮するのか、分子生物学的な機序が明らかとなった。