Myasthenia gravis is considered an autoimmune disease of the respiratory tract and muscle weakness of the body associated with the formation of antibodies against acetylcholine receptors (AChR) or related proteins (MuSK, lrp4, etc.) in the postsynaptic neuromuscular junction. Inflammatory and immunological mechanisms play an important role in the pathogenesis of MG; this article analyzes specifically inflammatory cellular processes, cytokines, and plasma mediators. It is known that the development of myasthenia gravis is not a full-fledged autoimmune disease, and the involvement of various cytokines in the pathogenesis has shown that the inflammatory process is at the heart of the disease