New developments in the immunopathogenesis of neuromuscular transmitter disorders

Myasthenia gravis is caused by an autoimmune process directed at the nicoti nic acetylcholine receptor of the skeletal muscle. Antibodies mediate both structural damage and functional blockade of the receptor at the postsynapt ic endplate. The fine specificity of the B- and T-cell responses to epitope s of the receptor molecule is well investigated. The thymus plays a particu lar role in both induction and perpetuation of the autoimmune process in my asthenia gravis. At the presynaptic site of the neuromuscular junction the Lambert-Eaton myasthenic syndrome is a complementary autoimmune disorder in duced by antibodies to calcium channels. This may occur as a paraneoplastic syndrome associated with small cell cancer of the lung.