Myasthenia gravis is probably the most thoroughly understood of all human autoimmune diseases. The basic mechanism of the disease is an antibody-mediated autoimmune attack that decreases the acetylcholine receptor density at the neuromuscular junction. Current therapies aim to restore the available acetylcholine receptors, deplete the autoantibodies or suppress the immune system. Prolonged drug treatment is required, but this carries a potential risk of severe adverse effects. Therefore, the ideal treatment for myasthenia would eliminate the abnormal autoimmune response without interfering with the immune system.