The mechanisms and its role of galectin-7 production system on epidermal keratinocyte in atopic dermatitis.

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K08747
• 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: Hamamatsu University School of Medicine
• Principal Investigator: Shimauchi Takatoshi 浜松医科大学, 医学部附属病院, 講師 (90399204)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: ガレクチン－７ / アトピー性皮膚炎 / 細胞接着 / IL-4 / IL-13 / Stat6 / alarmin / バリア機能障害

Outline of Final Research Achievements

We demonstrated that increased Gal-7 expression levels in both skin lesions and sera in atopic dermatitis (AD) patients. Furthermore, the serum Gal-7 levels could be a biomarker for AD patients. Our in vitro data also showed that IL-4/IL-13 facilitated the extracellular release of endogenous Gal-7 in keratinocytes via STAT6 signaling pathway, that contributes to protection against the disruption of cell adhesion. Our study unveils the characteristic of Gal-7 and its possible role as an alarmin that reflect the IL-4/IL-13-induced skin barrier impairment in AD.

Free Research Field

アトピー性皮膚炎

Academic Significance and Societal Importance of the Research Achievements

アトピー性皮膚炎におけるTh2誘導性の皮膚バリア機能障害がGal-7によって保護されている全く新しい概念を提唱する成果が得られた。これは病理学的、分子生物学的に重要であるばかりか、外的にGal-7を補い、皮膚バリア機能障害を改善させるという、アトピー性皮膚炎における新規外用剤の開発へとつながる可能性をも持つ。アトピー性皮膚炎に苦しむ患者は多く、学術的にも社会的にも大きな意義を持つ。