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gMG: an incapacitating, IgG-mediated autoimmune disease1-3

Generalized myasthenia gravis (gMG) is a chronic neuromuscular autoimmune disease driven by pathogenic immunoglobulin G (IgG) autoantibodies against key components of the neuromuscular junction (NMJ).1,4,5

For patients with gMG, the physical and psychological burdens can be severe and life-threatening3,6-8


gMG causes intense muscle weakness that often results in impaired mobility, speech, swallowing, and vision, as well as extreme fatigue.3,9


Up to 20% of patients experience myasthenic crisis, which can cause fatal respiratory failure.10,11

IgG autoantibodies target multiple components of the NMJ1,4,5

Pathogenic IgG autoantibodies targeting acetylcholine receptors (AChR), muscle-specific tyrosine kinase (MuSK), and low-density lipoprotein receptor-related protein 4 (LRP4) have been described in patients with gMG.4,5

What enables pathogenic IgG autoantibodies?


of patients have autoantibodies against AChR.5


of patients have autoantibodies against MuSK.4,5


of patients have autoantibodies against LRP4.4


of patients are seronegative, with no identifiable autoantibodies.4

FcRn plays a central role in IgG regulation12,13

The neonatal Fc receptor (FcRn) has been found to recycle IgG and to prolong its half-life, which maintains high concentrations of pathogenic IgG autoantibodies that attack vital components of the NMJ.1,5,12-15

When directed against AChR, IgG autoantibodies can often lead to the failure of neuromuscular transmission and skeletal muscle weakness through 3 distinct pathogenic actions.16,17

Is it time to take a closer look?

1. Functional blockade of AChR9,16,17

2. Internalization and degradation of AChR9,16,17

3. Activation of the complement system9,16,17

Discover the role of IgG autoantibodies and FcRn-mediated antibody recycling in gMG


References: 1. Rødgaard A et al. Clin Exp Immunol. 1987;67(1):82-88. 2. Jacob S. Eur Neurol Rev. 2018;13(1):18-20. doi.org/10.17925/ENR.2018.13.1.18 3. Twork S et al. Health Qual Life Outcomes. 2010;8:129. doi:10.1186/1477-7525-8-129 4. Gilhus NE. N Engl J Med. 2016;375(26):2570-2581. doi:10.1056/NEJMra1602678 5. Behin A, Le Panse R. J Neuromuscul Dis. 2018;5(3):265-277. doi:10.3233/JND-170294 6. Boldingh MI et al. Health Qual Life Outcomes. 2015;13:115. doi:10.1186/s12955-015-0298-1 7. Eliasen A, Dalhoff KP, Horwitz H. J Neurol. 2018;265(6):1303-1309. doi:10.1007/s00415-018-8837-4 8. Chu HT et al. Front Psychiatry. 2019;10:1-7. doi:10.3389/fpsyt.2019.0048 9. Gilhus NE et al. Nat Rev Neurol. 2016;12(5):259-268. doi:10.1038/nrneurol.2016.44 10. Grob D et al. Muscle Nerve. 2008;37(2):141-149. doi:10.1002/mus.20950 11. Wendell LC, Levine JM. Neurohospitalist. 2011;1(1):16-22. doi:10.1177/1941875210382918 12. Roopenian DC, Akilesh S. Nat Rev Immunol. 2007;7(9):715-725. doi:10.1038/nri2155 13. Ward ES, Ober RJ. Trends Pharmacol Sci. 2018;39(10):892-904. doi:10.1016/j.tips.2018.07.007 14. Ghetie V et al. Eur J Immunol. 1996;26(3):690-696. doi:10.1002/eji.1830260327 15. Ulrichts P et al. J Clin Invest. 2018;128(10):4372-4386. doi:10.1172/JCI97911 16. Huijbers MG et al. J Intern Med. 2014;275(1):12-26. doi:10.1111/joim.12163 17. Mantegazza R et al. Neuropsychiatr Dis Treat. 2011;7:151-160. doi:10.2147/NDT.S8915