Camp inhibits the okt3‐ induced increase in cytoplasmic free calcium in the jurkat t cell line: the degree of inhibition correlates inversely with the amount of cd3 binding ligand used*

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Abstract
We have investigated the effect of cAMP concentration on the CD3-mediated rise in intracellular Ca2+ induced by anti-CD3 monoclonal antibody in the human T cell leukemia line Jurkat. Forskolin, prostaglandin E2 (PGE2) and dibutyryl cAMP (db-cAMP) were used to increase intracellular cAMP concentrations. Treatment of Jurkat cells with forskolin or db-cAMP for 3 h inhibited the subsequent rise in intracellular Ca2+ concentration induced by an optimally mitogenic dose of 100 ng/ml of the anti-CD3 OKT3, whereas PGE2 counteracted the Ca2+ rise only marginally. The inhibitory effect of forskolin and PGE2 on the Ca2+ signal correlated with their abilities to induce increased cAMP levels in Jurkat cells. The suppression of the Ca2+ response was dependent on the concentration of the cAMP-elevating agent and the time of pre-incubation with the drug. The cAMP-mediated inhibition of the Ca2+ response diminished or disappeared when increasing concentrations of OKT3 were used to stimulate the rise in intracellular Ca2+ concentration. The results indicate that cAMP participates in the regulation of T lymphocyte activation at the level of signal transduction. Our findings, which stress the crucial role of the concentration of the ligand used to trigger Ca2+ responses, provide an explanation to previous contradictory reports on the impact of cAMP on the signal transduction in T cells.