Functional Characterization of HLA-G+ Regulatory T Cells in HIV-1 Infection

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Functional Characterization of HLA-G+ Regulatory T Cells in HIV-1 Infection

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Title: Functional Characterization of HLA-G+ Regulatory T Cells in HIV-1 Infection
Author: Li, Chun; Toth, Ilona; Schulze zur Wiesch, Julian; Pereyra, Florencia; Rychert, Jennifer Ann; Rosenberg, Eric Scott; van Lunzen, Jan; Lichterfeld, Mathias; Yu, Xu

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Citation: Li, Chun, Ilona Toth, Julian Schulze zur Wiesch, Florencia Pereyra, Jennifer Rychert, Eric S. Rosenberg, Jan van Lunzen, Mathias Lichterfeld, and Xu G. Yu. 2013. Functional characterization of hla-g+ regulatory t cells in hiv-1 infection. PLoS Pathogens 9(1): e1003140.
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Abstract: Regulatory T cells represent a specialized subpopulation of T lymphocytes that may modulate spontaneous HIV-1 disease progression by suppressing immune activation or inhibiting antiviral T cell immune responses. While the effects of classical CD25hi FoxP3+ Treg during HIV-1 infection have been analyzed in a series of recent investigations, very little is known about the role of non-classical regulatory T cells that can be phenotypically identified by surface expression of HLA-G or the TGF-β latency-associated peptide (LAP). Here, we show that non-classical HLA-G-expressing CD4 Treg are highly susceptible to HIV-1 infection and significantly reduced in persons with progressive HIV-1 disease courses. Moreover, the proportion of HLA-G+ CD4 and CD8 T cells was inversely correlated to markers of HIV-1 associated immune activation. Mechanistically, this corresponded to an increased ability of HLA-G+ Treg to reduce bystander immune activation, while only minimally inhibiting the functional properties of HIV-1-specific T cells. Frequencies of LAP+ CD4 Treg were not significantly reduced in HIV-1 infection, and unrelated to immune activation. These data indicate an important role of HLA-G+ Treg for balancing bystander immune activation and anti-viral immune activity in HIV-1 infection and suggest that the loss of these cells during advanced HIV-1 infection may contribute to immune dysregulation and HIV-1 disease progression.
Published Version: doi:10.1371/journal.ppat.1003140
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