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2015 Fiscal Year Final Research Report

Role of ARID5 in Rheumatoid Arthritis

Research Project

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Project/Area Number 26860744
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Collagenous pathology/Allergology
Research InstitutionChiba University

Principal Investigator

Furuta Shunsuke  千葉大学, 医学(系)研究科(研究院), 特任講師 (10422221)

Research Collaborator NAKAJIMA Hiroshi  
IKEDA Kei  
HANAOKA Hideki  
Project Period (FY) 2014-04-01 – 2016-03-31
Keywords内科 / 膠原病内科 / 関節リウマチ / ARID5 / CD4陽性T細胞
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.

Free Research Field

膠原病

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Published: 2017-05-10  

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