Apoptosis induced by HIV-gp120 in a Th1 clone involves the generation of reactive oxygen intermediates downstream CD95 triggering

Marina Radrizzani, Paola Accornero, Domenico Delia, Roland Kurrle, Mario P. Colombo

Research output: Contribution to journalArticle

Abstract

HIV-gp120 sensitizes Th1 clones from seronegative donors to apoptosis, which occurs through two distinct events: expression of CD95L followed by its interaction with CD95 to trigger cell death. gp120-apoptosis of the Th1 clone 103 was inhibited by Cyclosporin A, the PTK inhibitors Genistein and PNU152518, as well as the anti-oxidants Ascorbic Acid and Glutathione. Cyclosporin A interfered with CD95L expression, Ascorbic Acid and Glutathione inhibited cell death triggered by CD95/CD95L interaction; Genistein and PNU152518 acted on both steps. The occurrence of oxidative stress during CD95-dependent apoptosis was supported by the direct evidence of ROI production.

Original languageEnglish
Pages (from-to)87-92
Number of pages6
JournalFEBS Letters
Volume411
Issue number1
DOIs
Publication statusPublished - Jul 7 1997

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Keywords

  • Apoptosis
  • CD4 Th1 clone
  • gp120
  • HIV
  • PTK
  • ROI

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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