Calcium dependency of antigen-specific (T3-Ti) and alternative (T11) pathways of human T-cell activation.

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Abstract
Human T lymphocytes are activated by 2 lineage-specific surface components: the antigen/major histocompatibility complex receptor (T3-Ti) and the unrelated T11 molecule. Interaction of either of these with their respective ligands leads to T-cell proliferation via an interleukin 2 (IL-2) dependent autocrine mechanism. To begin to characterize the molecular details of the activation process, the role of Ca2+ was examined using human T-cell clones and monoclonal antibodies directed against their surface components. Within minutes of triggering either the T3-Ti or T11 molecule, there is a large increase in intracellular Ca2+ concentration, as measured by quin-2 fluorescence. This is essential for induction of T-cell proliferation in inducer, suppressor and cytotoxic clones, and, therefore, presumably is required at an early step in the autocrine growth pathway. Thus, chelating exogenous Ca2+ specifically inhibits proliferation triggered by anti-T3-Ti or anti-T11 monoclonal antibodies, but it does not affect triggering by exogenous IL-2. The Ca2+ ionophore A23187 can, by itself, initiate clonal proliferation.