The modulation of spontaneous and anti Ig stimulated motility of lymphocytes by cyclic nucleotides and adrenergic and cholinergic agents

Translational movement in B lymphocytes was stimulated by anti Ig antibody. Drugs that are presumed to elevate cyclic AMP stopped this stimulated motility. Such was the case with dibutyryl cAMP and theophylline, cholera enterotoxin, and isoproterenol, a β adrenergic agonist. Conversely, in the absence of anti immunoglobulin antibody, cyclic GMP and the cholinergic drugs acetylcholine and carbamylcholine increased spontaneous motility of lymphocytes, with the B class of lymphocytes demonstrating greater responsiveness. The increase in motility brought about by cholinergic drugs was totally stopped by atropine, suggesting that the B lymphocyte surface contains a cholinergic receptor. The inhibition of anti immunoglobulin stimulated movement produced by cyclic AMP was not observed if the cells were first incubated with colchicine, the microtubular disrupting drug. This suggests that the cyclic AMP decreased motility was brought about by the increased stabilization of microtubules. Lymphocyte motility was dissociable from other early events subsequent to binding of anti immunoglobulin antibodies: patching, capping, and endocytosis of complexes were unaffected by cyclic AMP, cyclic GMP, or drugs of the adrenergic or cholinergic systems.