Abstract
Abstract CD4+Foxp3+ T cells are generated either in the thymus for natural regulatory T cells, or in periphery for inducible Treg cells (iTregs), which differentiate from naïve T cell precursors. Both Tregs express Foxp3 albeit they differ in their plasticity and in their expression of certain genes. Transforming growth factor-β (TGF-β) and interleukin-2 are important for iTreg generation and maintenance, whereas proinflammatory cytokines such as IL-4 and IL-6 impair Foxp3 induction. Much has been learned regarding the transcriptional roles of TGF-β in determining the fate of iTregs; however, the limited focus if any on a translational mechanism by which TGF-β regulates the fate of functional T cells is somewhat myopic. We previously showed a novel translational mechanism for TGF-β regulation of EMT in mouse mammary gland epithelial cells whereby hnRNP E1 (E1) binds to a structural, 33-nucleotide TGF-β-activated translation element in the 3’ UTR of target transcripts and represses their translation. In this study, we found that E1 knockdown (E1KD) in naïve CD4+ T cells induces TGF-β signaling and upregulates expression of multiple TGF-β target molecules implicated in iTreg cell differentiation. Furthermore, E1KD CD4+ T cells bypass the need for TGF-β and express Foxp3. This study adds to our knowledge on a hitherto unrecognized translational mechanism by which TGF-β controls iTreg cell fate.
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