Markers of Favorable Response to Complement Inhibitors Therapy

Myasthenia gravis is an autoimmune neurological disease caused by autoantibodies primarily directed against components of the postsynaptic membrane of the neuromuscular junction. Approximately 85% of patients have antibodies directed against the acetylcholine receptor (anti-AChR). Anti-AChR antibodies act through three distinct mechanisms: 1. Activation of the classical complement pathway: Formation of membrane-attack complexes (MACs) results in the destruction of the postsynaptic membrane. 2. Mechanical blockade: Anti-AChR antibodies block the acetylcholine binding site on its receptor. 3. Internalization and lysosomal degradation: Bivalent IgG causes cross-linking of adjacent receptors leading to internalization and degradation of AChRs (antigenic modulation). Patient mortality has significantly reduced due to effective treatments preventing severe exacerbations of myasthenic sympto