2015 Fiscal Year Final Research Report
The pathogenic role of Arid5a in infection and autoimmunity.
Project/Area Number |
26860328
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Immunology
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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)
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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)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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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.
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Free Research Field |
免疫学(サイトカイン)
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