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Decline of miR-124 in myeloid cells promotes regulatory T cell development in HCV infection.

Decline of miR-124 in myeloid cells promotes regulatory T cell development in HCV infection.
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Ren JP, Wang L, Zhao J, Wang L, Ning SB, El Gazzar M, Moorman JP, Yao ZQ,


Ren JP, Wang L, Zhao J, Wang L, Ning SB, El Gazzar M, Moorman JP, Yao ZQ, (click to view)

Ren JP, Wang L, Zhao J, Wang L, Ning SB, El Gazzar M, Moorman JP, Yao ZQ,

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Immunology 2016 Oct 18() doi 10.1111/imm.12680

Abstract

Myeloid-derived suppressor cells (MDSCs) and microRNAs (miRNAs) contribute to attenuating immune responses during chronic viral infection; however, the precise mechanisms underlying their suppressive activities remain incompletely understood. We have recently shown marked expansion of MDSCs that promote regulatory T (Treg) cell development in patients with chronic hepatitis C virus (HCV) infection. Here we further investigated whether the HCV-induced expansion of MDSCs and Tregs is regulated by a miRNA-mediated mechanism. miRNA array analysis revealed that six miRNAs were up-regulated and six miRNAs were down-regulated significantly in myeloid cells during HCV infection. Real-time RT-PCR confirmed the down-regulation of miR-124 in MDSCs from HCV patients. Bioinformatic analysis suggested that miR-124 may be involved in the regulation of signal transducer and activator of transcription 3 (STAT-3), which was overexpressed in MDSCs from HCV patients. Notably, silencing of STAT-3 significantly increased the miR-124 expression, whereas reconstituting miR-124 decreased the levels of STAT-3, as well as IL-10 and TGF-β, which were overexpressed in MDCSs, and reduced the frequencies of Foxp3(+) Treg cells that were developed during chronic HCV infection. These results suggest that reciprocal regulation of miR-124 and STAT-3 in MDSCs promotes Treg cell development, thus uncovering a novel mechanism for the expansion of MDSC and Treg cells during HCV infection. This article is protected by copyright. All rights reserved.

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