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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Decline of miR-124 in Myeloid Cells Promotes Regulatory T-cell Development in Hepatitis C Virus Infection

Ren, Jun P., Wang, Lin, Zhao, Juan, Wang, Ling, Ning, Shun B., El Gazzar, Mohamed, Moorman, Jonathan P., Yao, Zhi Q. 18 October 2016 (has links)
Myeloid‐derived suppressor cells (MDSC s) and microRNA s (miRNA s) 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 MDSC s 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 MDSC s and Treg cells is regulated by an miRNA ‐mediated mechanism. The RNA array analysis revealed that six miRNA s were up‐regulated and six miRNA s were down‐regulated significantly in myeloid cells during HCV infection. Real‐time RT ‐PCR confirmed the down‐regulation of miR‐124 in MDSC s 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 MDSC s 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 interleukin‐10 and transforming growth factor‐β , which were overexpressed in MDCS s, 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 MDSC s promotes Treg cell development, thus uncovering a novel mechanism for the expansion of MDSC and Treg cells during HCV infection.

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