Identification of two serum components regulating the expression of T-lymphocyte function in childhood myasthenia gravis.

We studied serums and cells from nine children with myasthenia gravis to determine whether there were alterations in the distribution or function of different T-lymphocyte subpopulations. The low numbers of E-rosette-forming T lymphocytes and their failure to respond to antigen by producing normal suppressor T cells were correlated with the presence of an IgG antibody directed toward the theophylline-sensitive T-cell subset; this activity could be blocked by d-tubocurarine. Incubation of normal T lymphocytes with serum from patients rendered the cells "myasthenia-like" when assayed for E-rosettes and for antigen-induced suppressor-cell function. A second, non-IgG factor found in patients' serums had activity like that of thymic hormone and induced T-cell maturation in normal bone marrow. This factor was not inhibited by d-tubocurarine; its activity was strongest in the two patients most severely affected, and it disappeared after thymectomy in both these patients. We conclude that in childhood myasthenia gravis there may be two independent serum factors; one an IgG antibody directed at a subset of T lymphocytes, blocked by d-tubocurarine and apparently unaffected by thymectomy, and the other a thymus factor that induces T-lymphocyte maturation.