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T‐Cell Chemiluminescence
Author(s) -
BENICHOU G.,
KANELLOPOULOS J. M.,
MITENNE F,
GALANAUD P.,
LECA G.
Publication year - 1989
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.1365-3083.1989.tb01210.x
Subject(s) - jurkat cells , phytohaemagglutinin , biochemistry , cell culture , respiratory burst , microbiology and biotechnology , biology , t cell , intracellular , protein kinase c , monoclonal antibody , chemistry , antibody , signal transduction , immune system , immunology , in vitro , genetics
The binding of mitogenic lectins phytohaemagglutinin (PHA), concanavalin A (Con A) and/or of monoclonal antibodies to different receptors such as antigen receptor complex or CD2 on human T cells generates increases in the concentrations of inositol triphosphate (IP3) and cytoplasmic free calcium. This T lymphocyte requires the delivery of two signals; the first can be provided by specific monoclonal antibodies or by mitogenic lectins, and the second by a phorbol ester, phorbol myristate acetate (PMA). In other cells such as macrophages, the rise of intracellular calcium via the generation of IP3 and stimulation of protein kinase C can activate the phospholipase A 2 , a calcium‐dependent enzyme. This enzyme initiates the release of reactive oxygen intermediates and metabolites of arachidonic acid. In order to know whether this other metabolic pathway can be generated in T cells, we tested the capacity of different T‐cell lines and clones to produce superoxide anion after stimulation by the above‐mentioned activating agents. In this paper, we demonstrate that treatment of the Jurkat human cell line with Con A, PHA, and PMA results in a significant release of reactive oxygen metabolites. Of the various T‐cell lines and clones tested, only Jurkat exhibited an oxidative burst. Moreover, none of the antibodies tested (anti‐CD3, anti‐CD2, and anti‐CD28) and known to activate T cells, and none of the immune complexes was able to mediate such an effect. The existence of an oxidative metabolism in at least one T‐cell line suggests that T‐cell activation may in some instances use another metabolic pathway.