CD4 + interleukin 17 (IL-17)-producing helper T cells (T H17 cells) are instrumental in the immune response to pathogens. However, an overactive T H17 response results in tissue inflammation and autoimmunity, and therefore it is important to identify the molecular mechanisms that control the development of T H17 cells. IL-2 suppresses such development, but how IL-2 production is actively suppressed during T H 7 differentiation is not understood. Here we report that under T H17-polarizing conditions, the transcription factors STAT3 and AhR upregulated the expression of Aiolos, a member of the Ikaros family of transcription factors. Using Aiolos-deficient mice, we demonstrated that Aiolos silenced the Il2 locus, promoting T H17 differentiation in vitro and in vivo. Thus, we have identified a module in the transcriptional program of T H17 cells that actively limits IL-2 production and promotes their differentiation.
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