Signal transducing mechanisms involved in human T cell activation via surface T44 molecules. Comparison with signals transduced via the T cell receptor complex

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Abstract
Antibodies against the T44 surface molecule have been shown to activate human T cells to produce interleukin 2. The role of Ca2+ in the triggering of the interleukin 2‐producing Jurkat T cell line by anti‐T44 monoclonal antibody has been investigated. We show that activation is initiated by an increase in the concentration of free cytoplasmic calcium ions [Ca2+]i. Subsequently, we have investigated the mechanism by which perturbation of T44 molecules induces increases of [Ca2+]i in Jurkat cells. We show that the anti‐T44‐mediated increase in [Ca2+]i can occur only in presence of extracellular Ca2+, since no increment is detectable when extracellular Ca2+ is depleted by EGTA. Thus, it appears that perturbation of T44 molecules, unlike that of T3‐Ti antigen receptor complex, fails to mobilize Ca2+ from intracellular stores. As inositol triphosphate is considered the putative mobilizer of Ca2+ from internal stores, we measured the levels of inositol triphosphate and of the other inositol phosphate compounds in Jurkat cells after stimulation with anti‐T44 antibodies. In contrast to the stimulation via the T3‐Ti antigen receptor complex, stimulation via T44 molecule does not induce increments of all three inositol phosphates. Taken together, these data indicate that stimulation mediated by the T44 molecule proceeds via a mechanism independent from the typical inositol lipid metabolism which does not involve mobilization of Ca2+ from internal stores.