Exploring Upstream Targets to Optimize Myasthenia Gravis Treatment
Panelists discuss how myasthenia gravis is a T-cell–dependent, B-cell–mediated autoimmune disorder affecting neuromuscular transmission through different autoantibodies (acetylcholine receptor, MuSK, and LRP4) that target the neuromuscular junction through various mechanisms including complement activation and receptor clustering disruption.
Panelists discuss how seronegative patients may still have undetectable antibodies and respond to plasma exchange, suggesting serum factors are involved. They require different diagnostic approaches, including cell-based assays and genetic testing, to differentiate between congenital myasthenia and other disorders.
