Commentary on “Randomized trial of thymectomy in myasthenia gravis”

The relationship of the thymus to myasthenia gravis (MG) has been recognized at the very beginning of the last century (1,2). This relationship primarily applied to thymoma-associated MG (TAMG), in which thymectomies reportedly led to objective clinical improvement without the use of immunosuppressive drugs in the 1930-ies (3). Such TAMG cases account for approximately 10% of all MG, do not show a gender- or major histocompatibility complex (MHC) predilection, patients are elder than non-thymoma-associated MG affected individuals, and often have a specific set of anti-titin and anti-ryanodine receptor autoantibodies (4). There is experimental evidence that defective thymopoiesis (selection) of T-cells orchestrated by the neoplastic thymic epithelial cells, supported by a general cytokine network deregulation (5), are responsible for TAMG development; the neoplastic thymic epithelial cells finally being more limited (dysfunctional) to prevent export of autoreactive T-cells in the periphery.