Prostaglandin E2 inhibits T cell activation-induced apoptosis and Fas-mediated cellular cytotoxicity by blockade of Fas-ligand induction

Brian O. Porter, Thomas R. Malek

Research output: Contribution to journalArticle

40 Scopus citations

Abstract

Prostanoids exhibit both pro-apoptotic and anti-apoptotic functions depending on the maturation stage and tissue localization of target cells. Prostaglandin (PG) E2 has been shown to protect T lymphocytes from TCR-mediated activation-induced cell death, but the mechanism by which PGE2 inhibits apoptosis of T cells has not been established. We show that this protection involves the down-regulation of Fas-ligand (Fas-L) mRNA levels in T cells. Modulation of cell surface Fas-L expressin by physiological concentrations of PGE2 was shown to be both anti-apoptotic as well as capable of inhibiting Fas-L-mediated cytotoxicity of Fas-transfected P815 target cells. Thus, this study provides direct evidence of the likely biological means by which PGE2 down-regulates T cell apoptosis.

Original languageEnglish (US)
Pages (from-to)2360-2365
Number of pages6
JournalEuropean Journal of Immunology
Volume29
Issue number7
DOIs
StatePublished - Jul 17 1999

Keywords

  • Activation-induced cell death
  • Apoptosis
  • Fas ligand
  • Prostaglandin E
  • T cell

ASJC Scopus subject areas

  • Immunology

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