Characterization of lpr-derived T cell hybridomas: Fas-deficient hybridomas are deathless, growth-arrested, and cytotoxic upon activation

Cell Immunol. 1996 Feb 1;167(2):302-12. doi: 10.1006/cimm.1996.0039.


T cell hybridomas that are deathless upon TCR crosslinking were generated from lpr mice. The deathless hybridomas (1.4 and 5D5) expressed extremely low Fas even after anti-CD3 activation, whereas activation-induced cell death (AICD) was observed for Fas-expressing hybridomas. The deathless hybridomas were activated to produce FasL and IL-2, indicating that the intrinsic defect in Fas expression or up-regulation resulted in AICD blockade. The deathless hybridoma cells expressed longer and stronger FasL cytotoxicity than AICD-sensitive hybridomas. Although deathless, activated 5D5 cells were arrested at the G1/S border. Growth arrest lasted for at least 5 days, but some cells eventually recovered and proliferated. The deathless 5D5 cells were used to demonstrate that AICD includes a fratricidal mechanism that kills AICD-sensitive bystanders. The deathless T cell hybridomas are useful tools for studying T cell activation-dependent functions sensitive to AICD.

Publication types

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

MeSH terms

  • Animals
  • Base Sequence
  • Cell Death*
  • Cell Division
  • DNA Primers / chemistry
  • Fas Ligand Protein
  • Gene Expression
  • Hybridomas / pathology*
  • Lymphocyte Activation*
  • Membrane Glycoproteins / genetics
  • Mice
  • Mice, Mutant Strains
  • Molecular Sequence Data
  • RNA, Messenger / genetics
  • Receptors, Antigen, T-Cell / physiology
  • T-Lymphocytes / cytology*
  • T-Lymphocytes, Cytotoxic / cytology*
  • fas Receptor / physiology*


  • DNA Primers
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • RNA, Messenger
  • Receptors, Antigen, T-Cell
  • fas Receptor