All of the following statements are true about the pathogenesis of myasthenia gravis except:

E. Clinical improvement following thymectomy is correlated with decreased acetylcholine receptor antibody titers.

DISCUSSION: Myasthenia gravis is generally regarded as an autoimmune disorder due to antibodies directed toward the acetylcholine receptor. A variety of autoimmune mechanisms have been proposed; the ultimate result is a reduction in the number of functional acetylcholine receptors at the motor end plate. Proposed immune mechanisms include complementmediated receptor destruction, antibody-induced accelerated receptor turnover, and simple receptor blockade. In spite of these proposed immune mechanisms, the severity of myasthenia symptoms and improvement following therapy do not correlate with antibody titers. Although the source of these autoantibodies is not proven, it is generally felt that a nonspecific thymitis may trigger the autoantibody response, the thymic myoid cells serving as the source of the antigen.