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The TcR‐CD3 Complex is Required for Activation of Human Lymphocytes with Staphylococcal Enterotoxin A
Author(s) -
LANDO P. A.,
DOHLSTEN M.,
KALLAND T.,
SJOGREN H. O.,
CARLSSON R.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb02752.x
Subject(s) - cd3 , t cell receptor , phytohaemagglutinin , biology , cd8 , monoclonal antibody , enterotoxin , microbiology and biotechnology , t cell , antibody , immunology , antigen , lymphocyte , immune system , gene , biochemistry , escherichia coli
The involvement of the T‐cell receptor (TcR)‐CD3 complex in activation of human mononuclear cells by staphylococcal enterotoxin A (SEA) was investigated. TcR‐CD3 molecular complex expression was modulated with monoclonal anti‐CD3 antibodies. The proliferative response of such modulated cells to optimal doses of phytohaemagglutinin and monoclonal anti‐CD3 antibodies and to suboptimal doses of SEA was greatly impaired. In comcentrations above 1 ng/ml, SEA could also activate the modulated cells to a certain extent, apparently due to reexpression of low levels of the TcR‐CD3 molecular complex during incubation. TcR‐CD3 modulation decreased the ability of SEA‐activated cells to produce interleukin 2 and gamma interferon. Analysis of cloned cells revealed that SEA could only activate CD3 + but not CD3 clones. Both CD4 + and CD8 + clones were activated. The results show that sea activates human T cells by a mechanism involving the TcR‐CD3 molecular complex.