The symptoms of generalized myasthenia gravis (gMG) are generally perpetuated by IgG autoantibodies against acetylcholine receptors (AChR), muscle-specific tyrosine kinase (MuSK), and low-density lipoprotein receptor-related protein 4 (LRP4). Therefore, it may be worth exploring strategies that modulate the recycling of these IgG antibodies by FcRn.1,2
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References: 1. Roopenian DC, Akilesh S. Nat Rev Immunol. 2007;7(9):715-725. doi:10.1038/nri2155 2. Gilhus NE et al. Nat Rev Neurol. 2016;12(5):259-268. doi:10.1038/nrneurol.2016.44