The pathogenic role of Arid5a in infection and autoimmunity.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860328
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: Osaka University
• Principal Investigator: MASUDA Kazuya 大阪大学, 免疫学フロンティア研究センター, 寄附研究部門助教 (70722544)
• Research Collaborator: KISHIMOTO Tadamitsu 大阪大学, 免疫学フロンティア研究センター, 特任教授 (10093402) ; TAKEUCHI Osamu 京都大学, ウイルス研究所, 教授 (10379092)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 自己免疫疾患 / T細胞過剰活性化 / RNA安定性制御 / RNA結合タンパク質

Outline of Final Research Achievements

It has been reported that high expression of IL-6 is associated with the patients with rheumatoid arthritis. Recently, we found that AT-rich interactive domain containing 5a (Arid5a) stabilize IL-6 mRNA through binding to IL-6 3'UTR, which in turn elevates IL-6 level in vivo. In this study, we demonstrated that IL-6-induced Arid5a in T cells stabilized Stat3 mRNA by inhibiting the function of an RNAse Regnase-1, and thereby promoted the differentiation of Th17 cells. Thus, Arid5a contributes to elevation of IL-6 level in vivo, but also drives Th17 differentiation.

Free Research Field

免疫学(サイトカイン)