ACTIVATED B CELLS IN THE THYMUS GLAND OF PATIENTS WITH MYASTHENIA GRAVIS

Myasthenia gravis (MG) is an autoimmune disease caused by the production of autoantibodies that damage acetylcholine receptors (AchR) at the myoneuronal junction. It is well documented that abnormalities of the thymus gland, including lymphofollicular thymitis and thymoma, may play a role in the pathogenesis of this disease. Association between acetylcholine receptor autoantibodies and thymic changes such as lymphofollicular hyperplasia (LFH) have been widely discussed. Although LFH is not pathognomonic for MG, it is the most common pathologic finding. Germinal centers (GCs) found in MG patients are larger and more frequent than those in normal individuals.2 Previous studies revealed hyperactivity of B and T cells in MG. Expression of AchR in the thymus gland, hypersecretion of thymopoietin, and anarchism in the immunoregulatory mechanism involving B and T cells are other proposed mechanisms.