Dual role of TNF‐α in NK / LAK cell‐mediated lysis of chronically HIV‐infected U1 cells. Concomitant enhancement of HIV expression and sensitization of cell‐mediated lysis

The U937‐derived chronically HIV‐infected U1 cell line and uninfected U937 cell clones were efficiently lysed by both unstimulated (NK) and IL‐2‐stimulated (lymphokine‐activated killer; LAK) peripheral blood mononuclear cells (PBMC) of healthy HIV‐seronegative donors. Pretreatment of target cells with IFN‐γ down‐modulated killing of both U1 cells and two U937 cell clones, and up‐regulated MHC class I expression. In contrast, TNF‐α enhanced the sensitivity of infected U1 cells, but not of U937 cell clones to NK / LAK cell lysis. Co‐cultivation of IL‐2‐stimulated PBMC with U1 cells triggered expression and replication of HIV by cell‐cell contact, and this effect was inhibited by anti‐TNF‐α antibodies (Ab); virus production was partially inhibited by zidovudine. Of interest, anti‐TNF‐α Ab protected U1 cells from LAK cell activity. Thus, TNF‐α can induce HIV expression from chronically infected U1 cells, but also plays an important role in sensitizing these cells to lysis.

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