Identification of pathogenic T cells in atopic dermatitis lesions and their activation mechanism

2022 Fiscal Year Final Research Report

• Project/Area Number: 21K20918
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0903:Organ-based internal medicine and related fields
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: Kurihara Kazuo 浜松医科大学, 医学部, 助教 (40907961)
• Project Period (FY): 2021-08-30 – 2023-03-31
• Keywords: T細胞 / アトピー性皮膚炎

Outline of Final Research Achievements

There were abundant CD103+ T cells in the epidermis and dermis in atopic dermatitis lesions. CD103 is one of the phenotypes for resident memory T cells (TRM). TRM is a non-recirculating memory T cell and remains the same nonlymphoid lesion for a while.
TRM is thought to be deeply involved in the resistance and recurrence of AD lesions. And TRM is producing IL-22, which is associated with epidermal thickness, and IL-22-producing CD103+CD8+T cells are significantly correlated with epidermal thickness in AD lesions. It is suggested that TRM might be connected with epidermal thickness and activation in AD lesion.

Free Research Field

慢性炎症性皮膚疾患における免疫機構の解明

Academic Significance and Societal Importance of the Research Achievements

本研究での研究成果によって、再発・治療抵抗性を示しやすい慢性炎症性皮膚疾患の１つであるアトピー性皮膚炎に対して、病変部に存在するレジデントメモリーT細胞（TRM）が関与している可能性を示した。このレジデントメモリーT細胞の機能や活性化機能が解明され、抑制することができれば、治療に難渋する症例の病態解明につながるだけでなく、新しい治療法へと繋がると考える。