CD95 expression and CD95-mediated apoptosis of T cells in multiple sclerosis. No differences from normal individuals and no relation to HLA-DR2

J Neuroimmunol. 1998 Jan;81(1-2):168-72. doi: 10.1016/s0165-5728(97)00173-2.

Abstract

CD95-mediated apoptosis is a potent endogenous pathway of T cell elimination that has been suggested to be altered in multiple sclerosis (MS). MS is associated with the HLA-DR2, Dw2, DQ6 HLA class II haplotype. We have previously reported that T cell lines from HLA-DR2-positive individuals show enhanced production of tumor necrosis factor (TNF), a cytokine homologous to CD95 ligand, in response to specific antigen. Here we have studied CD95 expression and susceptibility to CD95-mediated apoptosis in peripheral blood mononuclear cells (PBMC) and activated T cells of 20 healthy individuals and 20 MS patients, half of whom were HLA-DR2-positive. MS patients did not differ from healthy individuals in either parameter. There was also no difference in CD95 expression or CD95-mediated apoptosis when MS patients and healthy individuals were grouped and compared according to HLA-DR status. These data reveal no differential regulation of PBMC/T cell apoptosis induced by CD95 receptor ligation in MS and show no impact of HLA-DR2 status on PBMC/T cell susceptibility to the same apoptotic stimulus. However, to assess the contribution of T cell apoptosis to the pathogenesis of MS further studies on other details of the complex system leading to T cell apoptosis are required.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Autoimmune Diseases / genetics
  • Autoimmune Diseases / immunology*
  • Disease Susceptibility
  • Gene Expression
  • HLA-DR2 Antigen / genetics*
  • Humans
  • Lymphocyte Activation
  • Multiple Sclerosis / genetics
  • Multiple Sclerosis / immunology*
  • T-Lymphocytes / pathology*
  • fas Receptor / biosynthesis
  • fas Receptor / genetics
  • fas Receptor / physiology*

Substances

  • HLA-DR2 Antigen
  • fas Receptor