Analysis of molecular mechanisms required for differentiation potential of naive T cells

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K22547
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 49:Pathology, infection/immunology, and related fields
• Research Institution: Okinawa Institute of Science and Technology Graduate University
• Principal Investigator: Ishikawa Hiroki 沖縄科学技術大学院大学, 免疫シグナルユニット, 准教授 (30648621)
• Project Period (FY): 2019-06-28 – 2021-03-31
• Keywords: T細胞 / 分化 / 転写制御 / RNA

Outline of Final Research Achievements

Naive CD4 T cells differentiate into diverse types of T helper cells or regulatory T cells and play a major role in immune responses. However, the mechanism that regulates multipotency of naive CD4 T cell remains largely unknown. In this study, using mice deficient for Junb RNA isoform (n-Junb) that is specifically expressed in naive CD4 T cells, we found that the loss of n-Junb results in increase of IL-17A expression in Th17 cells, which suggests that n-Junb may regulate ability of naive CD4 T cells to differentiate into Th17 cells.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

CD4+ T細胞は各種自己免疫疾患において重要な役割を担うがその分化・機能を制御する分メカニズムについては不明な点が多く残っている。本研究で明らかにしたn-Junb RNAによるTh17細胞の炎症性サイトカインの発現抑制は、自己免疫疾患を制御する新たなメカニズムであり、今後より詳細な解析を続けることで将来的に自己免疫疾患の新たな治療法の開発に貢献する可能性がある。