The ultrastructural immunopathology of myasthenia gravis

Appropriate electron cytochemical and immuno-electronmicroscopic probes were employed for the ultrastructural localization of immunoglobulin G (IgG), the third component of complement (C3), and the acetylcholine receptor protein (AChR) at the motor endplate in MG, in experimental autoimmune MG (EAMG), and in passively transferred EAMG. There is excellent morphologic evidence to indicate that both IgG and C3 bind to AChR at the endplate in MG and EAMG, that the abundance of the immune complexes is proportionate to the abundance of AChR that remains at the endplate, and that the impaired neuromuscular transmission is primarily caused by the AChR deficiency at the endplate. Antibody-dependent complement-mediated destruction of segments of the postsynaptic membrane represents one of the mechanisms that can result in AChR deficiency in MG and EAMG.