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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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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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 / 転写後調節 / IL-6 mRNA / STAT分子 / Th17細胞 / Arid5a / Regnase-1 / インフルエンザ / 感染・炎症 / サイトカインストーム |
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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Report
(3 results)
Research Products
(4 results)
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[Journal Article] Arid5a regulates naive CD4+ T cell fate through selective stabilization of Stat3 mRNA2016
Author(s)
Masuda, K., Ripley, B., Nyati, K., Dubey, P., Zaman, M., Hanieh, H., Hoga, M., Yamashita, K., Standley, D., Mashima, T., Katahira, M., Okamoto, T., Matsuura, Y., Takeuchi, O. and Kishimoto, T.
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Journal Title
Journal of Experimental Medicine
Volume: 213
Issue: 4
Pages: 605-619
DOI
Related Report
Peer Reviewed / Open Access
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