In a study of the role of Ca++ in the stimulation of activated T lymphocytes with interleukin 2 (IL-2) it was found that IL-2-induced proliferation can occur independently of extracellular calcium. Further, there was no correlation between triggering of DNA synthesis and an increase in free cytoplasmic calcium. However, IL-2 induced an increased uptake of 45Ca++ from the extracellular medium. Since there is no increase in free cytoplasmic calcium, it must be assumed that this is caused by an increase in membrane-associated calcium. Further, the calcium channel-blocking agent, verapamil, and TMB-8, a putative inhibitor of mobilization of calcium from intracellular pools, both exerted a dose-dependent inhibition of IL-2-induced DNA synthesis in activated T lymphocytes. We conclude that calcium is not a second messenger in activated T lymphocytes stimulated by IL-2, but our results indicate that calcium may play a role at membrane level.
Interleukin 2 (IL-2) was shown to induce a small but significant increase in the level of cGMP after 20 min stimulation and a subsequent fall after 1 h in activated T lymphocytes. No change in the level of cAMP was observed. Addition of the cyclic nucleotide analogues dbcAMP or dbcGMP did not stimulate DNA synthesis. On the contrary, IL-2-induced [3H]thymidine incorporation was inhibited by these drugs. Further, the phosphodiesterase inhibitor theophylline inhibited proliferation of activated T lymphocytes. Our results indicate that neither cAMP nor cGMP act as 'second messengers' for IL-2 but support the theory that cAMP is a negative regulator of cell proliferation.
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