CD52 expression on CD4+ T cells in HIV-positive individuals on cART

Fie Juhl Vojdeman, Julie Christine Gaardbo, Hans Jakob Hartling, Marco Gelpi, Malene Hove-Skovsgaard, Anders Elm Pedersen, Susanne Dam Nielsen

    Abstract

    Background: HIV persists in a latent state in quiescent CD4+ T cells preventing eradication of HIV. CD52 is a surface molecule modulated by HIV. We aimed at examining factors related to CD52 expression on CD4+ T cells in HIV-positive individuals and the impact of initiation of combination antiretroviral therapy (cART). Methods: Peripheral blood mononuclear cells from 18 HIV-positive individuals and 10 uninfected age- and sex-matched controls were examined by flow cytometry for CD38 and CD52 expression on CD4+ T cells. Stimulation assays were performed on 8 healthy blood donors to determine a cutoff for CD52 expression. Results: All examined CD4+ T cells expressed CD52. However, both CD4+ T cells with higher (CD52++) and with lower CD52 expression (CD52dim) were found in HIV-positive individuals compared to uninfected controls. Two % CD52dim cells defined groups of high and low CD52: the group of individuals with high CD52 had higher CD4 counts at baseline (447 vs. 54 cells/mL, P = 0.02) and higher increase in CD4 counts during follow-up compared with low CD52 (P = 0.02). After 12 months of cART, CD52 increased (median fluorescence intensity 4846 vs. 5621, P< 0.05), whereas CD38 decreased (median fluorescence intensity 1519 vs. 730, P< 0.0001). Conclusions: All HIV-positive individuals in this cohort had CD4+ T cells that expressed CD52. Higher CD4 counts were found in those with high CD52. Furthermore, an increase in CD52 was found after 12 months of cART, indicating that anti-CD52 antibodies may be more efficient for depletion of CD4+ T cells in HIV-positive individuals on cART.

    OriginalsprogEngelsk
    TidsskriftJournal of acquired immune deficiency syndromes (1999)
    Vol/bind77
    Udgave nummer2
    Sider (fra-til)217-220
    Antal sider4
    ISSN1525-4135
    DOI
    StatusUdgivet - 1 feb. 2018

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