Myasthenia gravis: immunological and clinical heterogeneity
We examine the current information on the epidemiology, immunopathogenesis, clinical manifestations, diagnosis, and treatment of myasthenia gravis, including developing therapies. It is established that is myasthenia gravis is an autoimmune disease in which the main targets there are elements of the neuromuscular synapse and intracellular structure of muscle fibers (antibodies to acetylcholine receptors, muscle-specific tyrosine kinase, low-density lipoprotein receptor-related protein 4, titin, and ryanodine receptors skeletal muscles). Their specificity and pathogenetic role in almost opened, but still remains about 15-20% of seronegative forms in which the classical clinical manifestations, most ocular myasthenia, have serological confirmation. Moreover, in patients with myasthenia determined and a number of related antibodies (antibodies to gangliosides, interleukin-12, interferon alpha-2 et al.), whose role is not precisely defined in the pathogenesis of myasthenia gravis and comorbid disorders. Pathophysiological result of this autoimmune process is the end-plate dysfunction neuromuscular synapses and the gradual addition of dynamic muscle weakness of the stationary component. With respect to clinical manifestations, there is a tendency to form patterns on the basis of clinical and immunological correlates of clinics and lessons learned on the effectiveness of therapeutic strategies in various forms, which allows more differentiated approach to the use of and search for new therapies.