APO-1(CD95)-dependent and -independent antigen receptor-induced apoptosis in human T and B cell lines

Marcus E. Peter*, Jens Dhein, Andreas Ehret, Stefan Hellbardt, Henning Walczak, Gerhard Moldenhauer, Peter H. Krammer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


Certain B and T cell lines respond to activation signals, e.g. through the antigen receptor, by undergoing apoptotlc cell death. In T cells it has been recently shown that TCR-mediated apoptosis involves APO-1/Fas (CD95) receptor-ligand interaction. To investigate whether the TCR-CD3 complex can trigger alternative apoptosis pathways we generated subclones of the T cell line Jurkat which were completely resistant towards APO-1-mediated apoptosis. These JurkatR cells differed phenotypically from sensitive parental JurkatS cells only by the lack of APO-1 protein expression. Although JurkatR cells responded normally to anti-CD3 stimulation by expression of APO-1 ligand they failed to undergo anti-CD3-induced apoptosis. Thus, in Jurkat cells APO-1 -mediated apoptosis was the main, and might be the only, mechanism for anti-CD3-induced cell death. However, BL-60 B cells, highly sensitive to anti-IgM-induced apoptosis, did not use the APO-1 receptor-ligand system because they failed to express APO-1 ligand mRNA. Taken together, our results suggest that malignant T and B cell lines may use APO-1 receptor-ligand-dependent and -independent antigen receptor-induced apoptosis pathways respectively. Similarly, differential pathways may be used by T and B cell subsets.

Original languageEnglish (US)
Pages (from-to)1873-1884
Number of pages12
JournalInternational Immunology
Issue number11
StatePublished - Nov 1995


  • APO-1
  • Apoptosis
  • Cytotoxicity
  • Fas

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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