Gli autoanticorpi IgA dimostrano un meccanismo innovativo di patologia della miastenia gravis MuSK.

Patients with muscle-specific tyrosine kinase (MuSK) myasthenia gravis (MG) develop muscle weakness due to functionally monovalent immunoglobulin (Ig) G4 autoantibodies (Abs) that target MuSK and disrupt acetylcholine receptor (AChR) clustering. Emerging evidence from other autoimmune conditions suggests that Abs of the IgA class-the archetypal immunoglobulin isotype at mucosal sites-may synergize with IgG Abs, contributing to pathology. In MuSK MG, however, the presence of disease-specific IgA Abs has not yet been recognized, limiting a broader understanding of IgG4-driven autoimmunity. To address this knowledge gap, we leveraged cell-based binding assays, patient-derived recombinant monocl