REQUIREMENT OF P56(LCK) IN T-CELL RECEPTOR CD3-MEDIATED APOPTOSIS ANDFAS-LIGAND INDUCTION JURKAT CELLS

Interaction of Fas (C95) 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 involv ement of protein tyrosine kinase (PTK) activity activity in this proce ss, the role of src family PTK p56lck (lck) is not known. we report he re that, contrary to wild type Jurkat, the lck-deficient mutant JCaM i s resistant to anti-CD3-induced apoptosis and fails to express Fas-L m RNA upon anti-CD3 treatment. However, both Jurkat and JCaM were found to constitutively express Fas and were equally sensitive to anti-Fas-m ediated apoptosis. If stimulated with PMA plus ionomycin, MCaM express ed Fas-L mRNA and underwent apoptosis. These findings indicate that p5 61ck is required for TCR/CD3-mediated Fas-L induction but not for the transduction of fas receptor-mediated death signal. (C) 1995 Academic Press, Inc.