PURPOSE OF REVIEW: Myasthenia gravis, a rare disorder of the neuromuscular 
transmission, is increasingly acknowledged as a syndrome more than as a single 
disease. This review summarizes recent advances in pathophysiology which confirm 
the disease heterogeneity, and may help find disease-targeted and 
patient-targeted therapies.
RECENT FINDINGS: Antibodies to the acetylcholine receptor, the muscle-specific 
tyrosine kinase and the lipoprotein receptor protein 4, characterize disease 
subtypes with distinct clinical traits and immune-pathogenic mechanisms. 
Genome-wide approaches have identified susceptibility loci within genes that 
participate in the immune response. Regulatory T and B cells appear to be 
defective in myasthenia gravis. In patients with acetylcholine receptor 
antibodies, thymectomy associated with prednisone proved more effective than 
prednisone alone in a multicenter randomized trial. New therapeutic options 
target B cells, B-cell growth factors and complement inhibition, and are 
currently reserved for patients with refractory disease.
SUMMARY: In the recent past, there has been an active search for new antigens in 
myasthenia gravis, whereas clinical and experimental studies have provided new 
insights of crucial pathways in immune regulation, which might become the 
targets of future therapeutic interventions.