Vitamin E inhibits CD95 ligand expression and protects T cells from activation-induced cell death

J Clin Invest. 2002 Sep;110(5):681-90. doi: 10.1172/JCI15073.

Abstract

Apoptosis is a morphologically distinct form of cell death involved in many physiological and pathological processes. Expression of the CD95 (APO-1/Fas) ligand (CD95L) is critically involved in activation-induced cell death (AICD) of activated T cells. Here we show that the natural free radical scavenger vitamin E suppresses the activity of the transcription factors NF-kappa B and AP-1, thus blocking expression of CD95L and preventing T cell AICD. Since AICD is a major cause of T cell depletion in AIDS, we examined 35 HIV-1-positive individuals and found that their T cells are more susceptible to AICD than are T cells isolated from healthy controls. Administration of vitamin E suppresses CD95L mRNA expression and protects T cells of HIV-1-infected individuals from CD95-mediated apoptosis. This evidence that vitamin E can affect T cell survival may merit further clinical investigation.

MeSH terms

  • Adult
  • Cell Death
  • Cell Nucleus / metabolism
  • Cell Survival
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Fas Ligand Protein
  • Female
  • HIV Seropositivity / metabolism
  • Humans
  • Jurkat Cells
  • Luciferases / metabolism
  • Lymphocyte Activation
  • Male
  • Membrane Glycoproteins / metabolism*
  • Middle Aged
  • NF-kappa B / metabolism
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocytes / cytology
  • T-Lymphocytes / metabolism*
  • Time Factors
  • Transcription Factor AP-1 / metabolism
  • Transcription, Genetic
  • Transfection
  • Vitamin E / metabolism
  • Vitamin E / pharmacology*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • NF-kappa B
  • RNA, Messenger
  • Transcription Factor AP-1
  • Vitamin E
  • Luciferases