Clinical utility of autoantibodies in the diagnosis and management of Myasthenia gravis

Myasthenia gravis is an autoimmune neuromuscular disease characterised by fatigable muscle weakness. The disease is caused by autoantibodies targeting components of the post-synaptic neuromuscular junction, which are identifiable in 90 % of cases. The most well-known and best-characterised of these is acetylcholine-receptor (AChR) antibody, which is present in approximately 50 % of ocular and 85 % of generalised MG patients. Other recognised pathogenic autoantibodies in MG target muscle specific kinase (MuSK) and low-density lipoprotein-receptor related protein 4 (LRP4), present in approximately 5–10 % and 1–5 % of MG cases respectively. Some autoantibodies are not directly pathogenic but inform disease severity and thymic status. Many other autoantibodies are described in MG, although their pathogenic role and clinical significance is yet to be determined. These include autoantibodies targeting COLQ, cortactin, rapsyn, AChE, and Kv1.4. In this review, we discuss the clinical utility of all autoantibodies implicated in MG to date, including their role in the diagnosis, management, and monitoring of the disease.