Inflammatory mechanism associated with impaired barrier function in atopic dermatitis

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K10216
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Tokyo Medical University
• Principal Investigator: YAMAMOTO Mami 東京医科大学, 医学部, 助教 (60421062)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: アトピー性皮膚炎 / インフラマゾーム

Outline of Final Research Achievements

Atopic dermatitis is a chronic inflammatory skin disease associated with impaired barrier function. In this study, we investigated the desiccation-associated inflammasome components and observed that the nucleotide-binding oligomerization domain-containing protein 2 (NOD2) may induce and the NOD-like receptor family pyrin domain containing 10 (NLRP10) may suppress inflammation. The activated NOD2 inflammasome triggers S100A9 protein synthesis, causes p38 and GATA3 phosphorylation, and promotes inflammation. These results suggest that the NOD2 inflammasome and its downstream effector S100A9 may play important roles in the pathogenesis of atopic dermatitis.

Free Research Field

皮膚科学

Academic Significance and Societal Importance of the Research Achievements

アトピー性皮膚炎の罹患者数は増加傾向にある。これまで炎症反応の抑制にはステロイド外用薬が多用されてきたが、近年、ヒト型抗ヒトIL-4/13受容体モノクローナル抗体などの生物学的製剤が開発され新たな治療選択が出てきている。本研究では、皮膚バリア障害の観点から炎症の惹起機構の解明を目的とし、さらにはその後の慢性化へと至るメカニズムの解明を目指したものであり、アトピー性皮膚炎の新たな治療法の糸口に結び付くものと考える。