| Project/Area Number |
26860744
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Chiba University |
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Principal Investigator |
Furuta Shunsuke 千葉大学, 医学(系)研究科(研究院), 特任講師 (10422221)
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| Research Collaborator |
NAKAJIMA Hiroshi
IKEDA Kei
HANAOKA Hideki
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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 | 内科 / 膠原病内科 / 関節リウマチ / ARID5 / CD4陽性T細胞 / ARID5A |
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| Outline of Final Research Achievements |
ARID5A was highly expressed in human and murine Th17 cells. Analysis with a Stat3 inhibitor and RORgt-deficient CD4 T cells revealed that the IL-6/Stat3 pathway directly induced ARID5A expression in CD4 T cells. Retrovirus-mediated induction of ARID5A in CD4 T cells resulted in the suppression of IL-17, IL-17F and IL-22 production but in the acceleration of IL-21 production. We also found that ARID5A directly bound to RORgt and inhibited RORgt-mediated suppression of IL-21 promoter activation, resulting in the acceleration of IL-21 expression. These results suggest that ARID5A functions as a switch molecule of IL-17-IL-21 balance in murine Th17 cells.
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