[Comment] Therapies for myasthenia gravis: FcRn inhibition and beyond

Myasthenia gravis is an antibody-mediated disease of the motor endplate that leads to impaired neuromuscular transmission.1 Pathogenic antibodies directed against antigens such as the postsynaptic acetylcholine receptor (AChR), muscle-specific tyrosine kinase (MuSK), and LDL receptor-related protein type 4 (LRP4) have been identified, each having a distinct pathogenic potential depending on the antigenic target and the IgG subtype.1,2 About 10% of patients are triple seronegative (ie, negative for antibodies to AChR, MuSK, and LRP4).

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