Antiganglioside
antibodies are frequently detected in sera from patients with autoimmune neuropathies, such as
Guillain-Barré syndrome,
Miller Fisher syndrome,
IgM paraproteinemic neuropathy, chronic inflammatory demyelinating
polyneuropathy, and multifocal motor neuropathy. In the acute phase sera from GBS patients, antiganglioside
antibodies are detected in 60-70%.
Ganglioside antigens recognized by serum
antibodies are varied from case to case.
IgG antibody against
GQ1b ganglioside is specifically raised in sera from patients with
Miller Fisher syndrome and
Guillain-Barré syndrome with
ophthalmoplegia. That antibody may bind to the paranodal myelin of oculomotor, trochlear and abducens nerves, where
GQ1b ganglioside is specifically localized, to cause
ophthalmoplegia.
IgM M-
protein which recognizes the disialosyl residue of GD1b is specifically associated with sensory ataxic neuropathy. The
IgM M-
protein may bind to the primary sensory neurons, where
GD1b ganglioside is localized, to cause sensory disturbance. After we confirmed the localization of GD1b in the rabbit primary sensory neurons, we sensitized rabbits with GD1b and induced sensory ataxic neuropathy in them. This is the first established animal model of autoimmune neuropathy induced by sensitization with
ganglioside. Some antiganglioside
antibodies may determine the clinical phenotype of neuropathy by binding specifically to the
ganglioside antigens which have unique localization.