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• W2404017401 startingPage "1767" @default.
• W2404017401 abstract "Objective: Autologous HIV-1-infected CD4+ primary T cells (aHIV+CD4) have been shown to be largely resistant to natural killer (NK)-cell-mediated lysis because of viral strategies of immune evasion. We have previously shown that a preactivation of NK cells with plasmacytoid dendritic cells can significantly augment lysis of aHIV+CD4 through a mechanism dependent on interferon-alpha (IFN-α). Design: The goal of the present study is to identify the specific NK-activating receptors involved in NK lysis of aHIV+CD4 following IFN-α activation. Methods: Peripheral blood mononuclear cells (PBMC) were incubated with aHIV+CD4 to induce the secretion of endogenous levels of IFN-α and drive NK activation. We then utilized a standard chromium lysis assay to assess the degree of IFN-α-activated lysis of aHIV+CD4 in the presence or absence of masking antibodies to a panel of NK-activating receptors and co-receptors. Results: Direct recognition of HIV-1-infected, but not uninfected, autologous CD4+ primary T cells by PBMC induced the secretion IFN-α (median 2280 pg/ml, P < 0.001, n = 9) that, in turn, activated NK cells (P < 0.001, n = 12) and significantly increased their cytolytic potential against aHIV+CD4 (P < 0.01, n = 12). The masking of NKp46 (P < 0.01, n = 8) and NKG2D (P < 0.05, n = 8), but not 2B4, NTBA, NKp30 or NKp44, significantly reduced IFN-α-activated lysis of aHIV+CD4. Conclusions: Taken together, these results demonstrate that endogenous levels of IFN-α secreted by plasmacytoid dendritic cells induce NK cells to lyse aHIV+CD4 via the engagement of NKp46 and NKG2D." @default.
• W2404017401 created "2016-06-24" @default.
• W2404017401 creator A5021041745 @default.
• W2404017401 creator A5069209710 @default.
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• W2404017401 date "2015-09-10" @default.
• W2404017401 modified "2023-09-26" @default.
• W2404017401 title "Lysis of HIV-1-infected autologous CD4+ primary T cells by interferon-alpha-activated NK cells requires NKp46 and NKG2D" @default.
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• W2404017401 doi "https://doi.org/10.1097/qad.0000000000000777" @default.
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