Arid5a regulates naive CD4+ T cell fate through selective stabilization of Stat3 mRNA.

Balance in signal transducer and activator of transcription activation is a key factor in regulating the fate of naive CD4(+)T cells. Here, we demonstrate that AT-rich interactive domain-containing protein 5a (Arid5a) in T cells directs naive CD4(+)T cells to differentiate into inflammatory CD4(+)T cells, especially Th17 cells, through selective stabilization ofStat3(but notStat1andStat5) mRNA in an IL-6-dependent manner. Loss of Arid5a in T cells led to reduction of level under Th17-polarizing conditions, whereas and in Arid5a-deficient T cells were highly activated compared with those of WT T cells under the same conditions. These cells displayed the feature of antiinflammatory (Il10-expressing) CD4(+)T cells. Thus, we show a T cell-intrinsic role of Arid5a on fate decisions of naive CD4(+)T cells through selective stabilization ofStat3mRNA.

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