ABSTRACT
Myasthenia gravis (MG) is an antibody-mediated, autoimmune neuromuscular disease in which autoantibodies directed against the nicotinic acetylcholine receptor (AChR) activate the complement cascade after binding to AChR. Antibody-and complementmediated destruction and/or cross-linking of AChR by antibodies, which lead to antigenic modulation, cause a reduction in the number of AChR molecules expressed at the neuromuscular junction (NMJ) (1-4). Anti-AChR antibodies can also bind to AChR and interfere with neuromuscular transmission (5). The above pathological events lead to neuromuscular transmission defects and culminate in weakness and fatigue of skeletal muscles in MG patients.
