Foxp3-driven miR-23~27~24 clusters control regulatory T cell-mediated immune regulation

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Abstract CD4+ Foxp3+ regulatory T (Treg) cells maintain immune homeostasis by regulating pathologic immune responses against self-, innocuous as well as dangerous foreign antigens. Previously, microRNA (miRNA)-mediated gene regulation has been shown to play a pivotal role in the maintenance and function of Treg cells. Here, we report that miR-23~27~24 clusters, which are abundantly expressed in Treg cells, are critical in controlling Treg cell biology. Foxp3 directly promotes elevated expressions of miR-23~27~24 clusters required for optimal Treg cell function through binding to the “enhancer element” at the miR-23~27~24 loci. Loss of miR-23~27~24 clusters in Treg cells lead to the development of spontaneous lympho-hyperactivation phenotypes over time. Moreover, upon allergen challenge, mice with Treg cell-specific ablation of miR-23~27~24 clusters exhibited elevated eosinophilic airway inflammation. Together, our results identify a Foxp3-driven miRNA family that plays important roles in controlling Treg cell-mediated immune regulation at both physiological and pathological settings.

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