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p56lck plays a key role in transducing apoptotic signals in T cells
Author(s) -
Di Somma M.Maddalena,
Nuti Sandra,
Telford John L.,
Baldari Cosima T.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00292-h
Subject(s) - jurkat cells , t cell receptor , apoptosis , microbiology and biotechnology , t cell , signal transduction , priming (agriculture) , biology , transfection , cell culture , cytotoxic t cell , zap70 , tyrosine kinase , biochemistry , immunology , in vitro , immune system , botany , germination , genetics
The CD4 receptor synergizes with the T‐cell antigen receptor (TCR) in helper T‐cell activation. However CD4 crosslinking in the absence of simultaneous TCR engagement leaves the cells primed to activation dependent apoptosis. To assess the role of the CD4 associated protein tyrosine kinase p56lck in CD4 priming to apoptosis we have constructed Jurkat T‐cell lines stably transfected with a constitutively active form of p56lck. These cells were constitutively primed to undergo apoptosis upon TCR crosslinking with specific antibodies. In addition the Jurkat JCaM1 line, which is defective for p56lck expression, was resistant to TCR induced apoptosis. These data indicate that p56lck is required for T‐cell apoptosis and that CD4 priming of T‐cells for antigen dependent apoptosis is due to inappropriate or partial activation of the p56lck signal transduction pathway.