Abstract

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.

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