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- W2321949008 abstract "Regulatory T cells (Tregs) are characterized by the expression of CD25 and FOXP3, the latter being essential for their development and function. Another major player in the regulatory function is the CTLA-4 surface molecule that inhibits cytotoxic responses. Despite this, the regulation of CTLA-4 expression remains less well explored than that of FOXP3. We therefore studied the microRNA signature of peripheral blood (PB) CD4+CD25+CD127low Tregs isolated from healthy volunteers, with a special focus on FOXP3 and CTLA-4 regulation, and we also studied their transcriptional profile. We confirmed that the investigated population was indeed a regulatory one (high expression of CTLA-4, FOXP3, IL-2 receptor and exhibition of a suppressive function) and pointed at other crucial genes expression that could be in the future subject of investigations. We identified a signature composed of fifteen differentially expressed microRNAs. Among those, miR-24, miR-145 and miR-210 were down regulated in Tregs compared to controls; miR-24 and miR-210 negatively regulated FOXP3 expression by binding directly to two target sites in its 3’UTR. On the other hand, miR-95, which is highly expressed in PB Tregs, positively regulated FOXP3 expression via an indirect mechanism yet to be identified. Finally, we showed that miR-145 negatively regulated CTLA-4 expression in human CD4+ PB Tregs by binding to its target site in CTLA-4 transcript 3’UTR. To our knowledge, this is the first characterization of human PB CD4+ Tregs. Moreover, unveiling one mechanism regulating CTLA-4 expression is novel and may lead to a better understanding of the regulation of this crucial gene." @default.
- W2321949008 created "2016-06-24" @default.
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- W2321949008 date "2013-04-01" @default.
- W2321949008 modified "2023-10-18" @default.
- W2321949008 title "ST113 Human CD4+CD25+CD127low Regulatory T cells" @default.
- W2321949008 doi "https://doi.org/10.1097/01.qai.0000429275.20963.cb" @default.
- W2321949008 hasPublicationYear "2013" @default.
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