| Abstract: | Myasthenia gravis may result from a reduction of available acetylcholine receptors at the neuromuscular junction, likely secondary to the presence of anti-acetylcholine receptor antibodies. Since T lymphocytes appear to carry a similar nicotinic acetylcholine receptor, we investigated the capacity of T cells from patients with myasthenia gravis to bind sheep erythrocytes. In addition we determined the effect of carbachol, a cholinergic agonist, on E-rosette formation, and the role of myasthenic serum in modulating these responses. Two groups of patients were identified; one with normal numbers of E-rosettes forming cells (E-RFC) and the other with significantly reduced numbers. The majority of patients with myasthenia had a reduced number of carbachol-sensitive T cells. Incubation of their serum (or the IgG fraction) with normal T cells led to a reduction in numbers of E-RFC, particularly of the carbachol-sensitive subset. These effects were blocked by d-tubocurarine and not by atropine. Following plasmapheresis, normal numbers of E-RFC were detected in the patients and the serum inhibitory activity was no longer detected. The data suggest that in parallel to the achievement of some degree of clinical improvement, plasmapheresis may restore some aspects of lymphocyte function. |
