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The Modulation of Spontaneous and Anti-Ig-Stimulated Motility of Lymphocytes by Cyclic Nucleotides and Adrenergic and Cholinergic Agents¹

From the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Abstract

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 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.

Footnotes

¹ This study was supported by National Institutes of Health Grant AI-10091.

² George Schreiner is supported by a Karin Grunebaum Cancer Research Foundation Fellowship.

³ Emil Unanue is a recipient of a Research Career Award from the National Institutes of Health.