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DURING the past five years data relevant to the hypothesis that myasthenia gravis might be caused by or intimately related to immunologic aberrations have been brought forward.1 , 2 Strauss et al.3 demonstrated in vitro a skeletal muscle-binding, complement-fixing serum globulin in some patients with myasthenia gravis. This reactivity was subsequently shown to be associated with the serum immunoglobulins. Beutner and his associates4 confirmed these findings. More recently, van der Geld et al.5 reported that myasthenic serums containing antimuscle reactivity also react with thymic epithelial cell cytoplasmic elements. Reciprocal absorption studies with skeletal muscle and thymus tissues demonstrated common antigenic determinants in . . .
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McFarlin et al. (1966) studied this question.
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