Abstract
Complement‐fixing antibodies to peripheral nerve myelin (anti‐PNM Ab) can be detected in the serum of patients with Guillain‐Barré syndrome (GBS). Kinetics of these antibodies can be correlated with the changing clinical course; the appearance of activation products of the terminal complement cascade in cerebrospinal fluid, serum, and peripheral nerve of patients with GBS; and the ability of GBS serum to mediate complement‐dependent demyelination of myelinating cultures of rodent dorsal root ganglion. Some of the anti‐PNM Ab in all GBS serum tested thus far bind a neutral glycolipid of human PNM and cross react with Forssman antigen, a cross‐species antigen found in many infectious agents. Studies suggest that an IgM antibody in GBS patients that could be triggered by multiple infectious agents binds a surface determinant of a Forssman‐like lipid of human PNM and participates in demyelination of peripheral nerve through the activation of complement.