Serum
antibodies against
glycolipids, mainly
gangliosides, are detected in about 60% of patients with
Guillain-Barré syndrome (GBS) and its variants. Anti-
glycolipid antibodies play a crucial role in the pathogenic mechanisms of GBS. The antibody titer is the highest in the acute phase and decreases gradually. Molecular mimicries occur between the
glycolipids and surface molecules on the infectious agents. Clinical subtypes of GBS are related to the antigenic specificities of the
antibodies. The distribution of
gangliosides in peripheral nervous tissues could explain the different clinical manifestations. The anti-GQ1b antibody is detected in 80-90% of patients with
Fisher syndrome characterized by
ophthalmoplegia. GQ1b is localized in the paranodes of the human cranial nerves innervating the extraocular muscles. This is consistent with the clinical association between the anti-GQ1b antibody and
ophthalmoplegia. The anti-GM1 antibody is associated with acute motor axonal neuropathy, whereas the anti-GD1b antibody is detected in acute sensory ataxic neuropathy. GBS animal models sensitized by
gangliosides, such as GM1 or GD1b, develop monophasic
peripheral neuropathies. In the animal models, disruption of molecule clusters and deposition of
complement products were observed in the nodal and paranodal regions. Clinical and experimental data suggest
complement-mediated pathogenic mechanisms triggered by anti-
glycolipid antibodies in GBS.