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.