Carbamycholine modulation of E-rosette formation: identification of nicotinic acetylcholine receptors on a subpopulation of human T lymphocytes.
We previously suggested that a population of T-suppressor cells carries acetylcholine receptors which may be involved in the regulation of the immune response. To identify cholinergic receptors on human T lymphocytes, we investigated the effects of carbachol, a cholinergic agonist, on E-rosette formation. Preincubation of normal human peripheral blood cells with carbachol resulted in a 30-40% reduction in numbers of E rosette-forming cells. Carbachol-induced inhibition of E-rosette formation was dose-dependent, temperature dependent, and reversible. The drug effects appeared to be mediated through a nicotinic acetylcholine receptor since d-tubocurarine (but not atropine) abrogated its activity. The expression of nicotinic receptors on a subset of human T cells may play an important role in the pathogenesis of certain diseases such as myasthenia gravis.
D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D004912:Erythrocytes / Q000276:immunology*; D006801:Humans; D066298:In Vitro Techniques; D008094:Lithium / Q000494:pharmacology; D009157:Myasthenia Gravis / Q000209:etiology; D009928:Organ Specificity; D011950:Receptors, Cholinergic / Q000187:drug effects*; D011978:Receptors, Nicotinic / Q000187:drug effects*; D012397:Rosette Formation; D012756:Sheep; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism
D011950:Receptors, Cholinergic; D011978:Receptors, Nicotinic; D002217:Carbachol; D008094:Lithium