Journal
NATURE IMMUNOLOGY
Volume 13, Issue 8, Pages 770-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2363
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Funding
- US National Institutes of Health [P01AI073748, P01NS038037, P01AI056299, R01NS030843, AI075285, AI093903]
- National Multiple Sclerosis Society [RG4111A1, FG1850-A-1]
- Harvard Medical School Office for Diversity and Community Partnership
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CD4(+) interleukin 17 (IL-17)-producing helper T cells (T(H)17 cells) are instrumental in the immune response to pathogens. However, an overactive T(H)17 response results in tissue inflammation and autoimmunity, and therefore it is important to identify the molecular mechanisms that control the development of T(H)17 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(H)17-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(H)17 differentiation in vitro and in vivo. Thus, we have identified a module in the transcriptional program of T(H)17 cells that actively limits IL-2 production and promotes their differentiation.
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