| Literature DB >> 27438767 |
Huang-Yu Yang1, Joseph Barbi2, Chao-Yi Wu3, Ying Zheng4, Paolo D A Vignali5, Xingmei Wu4, Jin-Hui Tao5, Benjamin V Park5, Shashika Bandara5, Lewis Novack5, Xuhao Ni5, Xiaoping Yang5, Kwang-Yu Chang6, Ren-Chin Wu7, Junran Zhang8, Chih-Wei Yang9, Drew M Pardoll5, Huabin Li10, Fan Pan11.
Abstract
Regulatory T (Treg) cells are important in maintaining self-tolerance and immune homeostasis. The Treg cell transcription factor Foxp3 works in concert with other co-regulatory molecules, including Eos, to determine the transcriptional signature and characteristic suppressive phenotype of Treg cells. Here, we report that the inflammatory cytokine interleukin-6 (IL-6) actively repressed Eos expression through microRNA-17 (miR-17). miR-17 expression increased in Treg cells in the presence of IL-6, and its expression negatively correlated with that of Eos. Treg cell suppressive activity was diminished upon overexpression of miR-17 in vitro and in vivo, which was mitigated upon co-expression of an Eos mutant lacking miR-17 target sites. Also, RNAi of miR-17 resulted in enhanced suppressive activity. Ectopic expression of miR-17 imparted effector-T-cell-like characteristics to Treg cells via the de-repression of genes encoding effector cytokines. Thus, miR-17 provides a potent layer of Treg cell control through targeting Eos and additional Foxp3 co-regulators.Entities:
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Year: 2016 PMID: 27438767 PMCID: PMC4957244 DOI: 10.1016/j.immuni.2016.06.022
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745