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

Claudio Fortis, Priscilla Biswas, Laura Soldini, Fabrizio Veglia, Anna Maria Careddu, Fanny Delfanti, Barbara Mantelli, Michelangelo Murone, Adriano Lazzarin, Guido Poli

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
Pages (from-to)3654-3662
Number of pages9
JournalEuropean Journal of Immunology
Volume29
Issue number11
DOIs
Publication statusPublished - 1999

Keywords

  • HIV
  • IFN-γ
  • Latency
  • NK
  • TNF-α

ASJC Scopus subject areas

  • Immunology

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