Abstract
Myasthenia gravis (MG) is a prototype of antibody-mediated autoimmune disease in which the immune pathogenesis seems to be well elucidated. However, the role of thymic abnormality in the pathogenesis remains uncertain. Thymectomy is effective for treatment in MG, but the theoretical evidence has not been established. In patients with MG with non-thymoma, it should be particularly important to show the rationale of thymectomy for treatment.
Acetylcholine receptor on thymic myoid cells was believed to trigger the autoimmune response in MG. However, subsequent studies have failed to support this hypothesis. Instead, thymic epithelial cells became important in the pathogenesis. The thymus of MG patients contains all cellular components required for the initiation of a myasthenogenic autoimmune reaction (i, e., antigen, antigenpresenting cells, autoreactive T and B cells, are present in the MG thymus), which is, so far, a major theoretical reason to support the thymectomy. The thymic abnormality is directory involved in the pathogenesis of MG, and the more elucidation of the details of complex interaction between the each element in the thymus should also lead to the further understanding of other autoimmune dis-orders.