Pathophysiology and immunological profile of myasthenia gravis and its subgroups

- Myasthenia gravis is an antibody-mediated disease.
- Antibodies in myasthenia gravis are directed against several postsynaptic neuromuscular proteins and epitopes.
- Thymus pathology is inducing myasthenia gravis.
- Autoantibody profile, thymus involvement and clinical manifestations vary between myasthenia gravis subgroups.
- Therapeutic response in myasthenia gravis is linked to subgroup and disease mechanisms.

Myasthenia gravis (MG) is an autoimmune antibody-mediated disease characterized by muscle weakness and fatigability. It is believed that the initial steps triggering humoral immunity in MG take place inside thymic tissue and thymoma. The immune response against one or several epitopes expressed on thymic tissue cells spills over to neuromuscular junction components sharing the same epitope causing humoral autoimmunity and antibody production. The main cause of MG is acetylcholine receptor antibodies. However, many other neuromuscular junction membrane protein targets, intracellular and extracellular proteins are suggested to participate in MG pathophysiology. MG should be divided into subgroups based on clinical presentation and immunology. This includes onset age, clinical characteristics, thymic pathology and antibody profile. The immunological profile of these subgroups is determined by the antibodies present.