Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas

Nature. 1995 Feb 2;373(6513):441-4. doi: 10.1038/373441a0.


A number of murine T-cell hybridomas undergo apoptosis within a few hours of activation by specific antigens, mitogens, antibodies against the T-cell antigen receptor, or a combination of phorbol ester and calcium ionophore. This phenomenon has been extensively studied as a model for clonal deletion in the immune system, in which potentially autoreactive T cells eliminate themselves by apoptosis after activation, either in the thymus or in the periphery. Here we show that the Fas/CD95 receptor, which can transduce a potent apoptotic signal when ligand, is rapidly expressed following activation of T-cell hybridomas, as is its functional, membrane-bound ligand. Interference with the ensuing Fas/Fas-ligand interaction inhibits activation-induced apoptosis. Because T-cell receptor ligation can induce apoptosis in a single T hybridoma cell, we suggest that the Fas/Fas-ligand interaction can induce cell death in a cell-autonomous manner.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, Surface / physiology*
  • Apoptosis / physiology*
  • Base Sequence
  • DNA
  • Endopeptidases / metabolism
  • Humans
  • Hybridomas
  • Ligands
  • Lymphocyte Activation*
  • Mice
  • Molecular Sequence Data
  • Recombinant Fusion Proteins
  • T-Lymphocytes / immunology
  • T-Lymphocytes / physiology*
  • fas Receptor


  • Antigens, Surface
  • Ligands
  • Recombinant Fusion Proteins
  • fas Receptor
  • DNA
  • Endopeptidases