Nicotine induces T-suppressor cells: modulation by the nicotinic antagonist D-tubocurarine and myasthenic serum.
To further unravel the basic immunoregulatory defect present in myasthenia gravis, we undertook to study nicotinic acetylcholine receptor (AchR) activity on human peripheral blood leukocytes. A biphasic suppressive effect of nicotine was observed on lymphocyte proliferative responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen with peaks at 10(-9) and 10(-5) M. Using a coculture approach, T cells preincubated with nicotine for 24 hr showed enhanced suppressor cell activity. This was partially blocked by serum from myasthenic patients and by the nicotinic antagonist d-tubocurarine. These studies suggest that suppressor T lymphocytes bear functional nicotinic AchR, which may be modulated by myasthenic serum, with possible relevance to the pathogenesis of myasthenia gravis.
D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000097:blood / Q000276:immunology; D002478:Cells, Cultured; D003864:Depression, Chemical; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D008934:Mitogens / Q000494:pharmacology; D009157:Myasthenia Gravis / Q000097:blood* / Q000276:immunology; D009538:Nicotine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011978:Receptors, Nicotinic / Q000187:drug effects* / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology; D014403:Tubocurarine / Q000494:pharmacology*
D001323:Autoantibodies; D008934:Mitogens; D011978:Receptors, Nicotinic; D009538:Nicotine; D014403:Tubocurarine