Thiols prevent Fas (CD95)-mediated T cell apoptosis by down-regulating membrane Fas expression

Eur J Immunol. 1996 Dec;26(12):2981-8. doi: 10.1002/eji.1830261225.

Abstract

Thiol antioxidants have been shown to protect cells against apoptosis. Based on the role of Fas in T cell apoptosis, we investigated the effect of thiols on Fas expression. We report that the thiol N-acetyl-L-cysteine (NAC) prevents the induction of Fas on human peripheral blood T cells in a dose-dependent manner. It also down-regulates in a time- and dose-dependent manner Fas expression on Fas-expressing T cells. Although these effects were not mediated through de novo glutathione synthesis, only compounds with a free thiol group decreased membrane Fas expression. The decrease of Fas expression induced by NAC was not associated with a modulation of Fas mRNA transcription nor with an internalization, suggesting that NAC may affect the processing of Fas. Indeed, a soluble immunoreactive form of Fas was detected by ELISA and by Western blotting in the supernatants of Fas-expressing T cells treated with NAC. As a functional consequence, NAC partly protected Jurkat cells against Fas-mediated apoptotic cell death. Thus, this study shows that, by regulating Fas expression, the cytoprotective properties of NAC can be extended to Fas-mediated cell death.

MeSH terms

  • Acetylcysteine / pharmacology*
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / immunology
  • Down-Regulation / drug effects*
  • Humans
  • Jurkat Cells
  • Membrane Proteins / biosynthesis*
  • T-Lymphocytes / drug effects*
  • fas Receptor / biosynthesis*
  • fas Receptor / drug effects*

Substances

  • Antioxidants
  • Membrane Proteins
  • fas Receptor
  • Acetylcysteine