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    Immunosenescent CD57 +CD4+ T-cells accumulate and contribute to interferon-γ responses in HIV patients responding stably to ART

    233619_233619.pdf (1.397Mb)
    Access Status
    Open access
    Authors
    Fernandez, S.
    French, M.
    Price, Patricia
    Date
    2011
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Fernandez, S. and French, M. and Price, P. 2011. Immunosenescent CD57 +CD4+ T-cells accumulate and contribute to interferon-γ responses in HIV patients responding stably to ART. Disease Markers. 31 (6): pp. 337-342.
    Source Title
    Disease Markers
    DOI
    10.3233/DMA-2011-0847
    ISSN
    0278-0240
    School
    School of Biomedical Sciences
    Remarks

    This open access article is distributed under the Creative Commons license http://creativecommons.org/licenses/by/3.0/

    URI
    http://hdl.handle.net/20.500.11937/4217
    Collection
    • Curtin Research Publications
    Abstract

    HIV-infected individuals responding to antiretroviral therapy (ART) after severe CD4+ T-cell depletion may retain low responses to recall antigens [eg: cytomegalovirus (CMV)] and altered expression of T-cell co-stimulatory molecules consistent with immunosenescence. We investigated the capacity of phenotypically senescent cells to generate cytokines in HIV patients receiving long-term ART (n = 18) and in healthy controls (n = 10). Memory T-cells were assessed by interferon (IFN)-γ ELISpot assay and flow cytometrically via IFN-γ or IL-2. Proportions of CD57brightCD28null CD4+ T-cells correlated with IFN-γ responses to CMV (p = 0.009) and anti-CD3 (p = 0.002) in HIV patients only. Proportions of CD57brightCD28null CD8+ T-cells and CD8+ T-cell IFN-γ responses to CMV peptides correlated in controls but not HIV patients. IL-2 was predominantly produced by CD28+T-cells from all donors, whereas IFN-γ was mostly produced by CD57+ T-cells. The findings provide evidence of an accumulation of immunosenescent T-cells able to make IFN-γ. This may influence the pathogenesis of secondary viral infections in HIV patients receiving ART.

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