Autoantibody in GBS and CIDP : Anti–glycolipid antibody

Abstract

Antibodies to glycolipid are detected in approximately 60% of Guillain–Barré syndrome (GBS) patients. Localizations of those antigens in human peripheral nerves are well correlated with clinical phenotypes of GBS. Campylobacter jejuni and Mycoplasma pneumoniae as antecedent infectious agents in GBS have carbohydrate structures mimicking glycolipids. Thus, anti–glycolipid antibodies, which are produced by antecedent infections, bind to glycolipids localized in human peripheral nerves and can cause GBS. By contrast to GBS, positive rate of anti–glycolipid antibodies is low in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Among glycolipids, LM1 is predominantly localized in human peripheral nerve myelin. LM1–related antibodies are detected in approximately 10% of CIDP patients. CIDP patients with those antibodies frequently present ataxia but rarely have cranial nerve deficits ; these features are possibly associated with the localization of LM1, which is more abundant in the dorsal root than the cranial nerves. Those findings suggest an involvement of anti–glycolipid antibodies–mediated mechanism in GBS and CIDP.