Requirement of P56lck in T-Cell Receptor CD3-Mediated Apoptosis and Fas-Ligand Induction Jurkat Cells

Naoki Oyaizu, Soe Than, Thomas W. McCloskey, Savita Pahwa

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


Interaction of Fas (CD95) and its ligand (Fas-L) has been shown to play a pivotal role in T cells receptor (TCR)/CD3 activation-induced cell death via apoptosis. Although several lines of evidence suggest involvement of protein tyrosine kinase (PTK) activity in this process, the role of src family PTK p56lck (lck) is not known. We report here that, contrary to wild type Jurkat, the lck-deficient mutant JCaM is resistant to anti-CD3-induced apoptosis and fails to express Fas-L mRNA upon anti-CD3 treatment. However, both Jurkat and JCaM were found to constitutively express Fas and were equally sensitive to anti-Fas-mediated apoptosis. If stimulated with PMA plus ionomycin, JCaM expressed Fas-L mRNA and underwent apoptosis. These findings indicate that p56lck is required for TCR/CD3-mediated Fas-L induction but not for the transduction of Fas receptor-mediated death signal.

Original languageEnglish (US)
Pages (from-to)994-1001
Number of pages8
JournalBiochemical and biophysical research communications
Issue number3
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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