Infectious origins of, and molecular mimicry in, Guillain-Barré and Fisher syndromes.
Guillain-Barré syndrome (GBS), characterised by limb weakness and areflexia, is the prototype of postinfectious autoimmune diseases, and Campylobacter jejuni is the most frequent antecedent pathogen. GBS subsequent to C jejuni enteritis is associated with a severe, pure motor axonal variant and IgG antibodies against GM1, GM1b, GD1a, or GalNAc-GDla, gangliosides expressed in human peripheral nerves. Lipopolysaccharides of C jejuni isolated from GBS patients have ganglioside-like epitopes. Cytomegalovirus is the most common viral antecedent infection. Patients with demyelinating GBS who have had a recent CMV infection have severe sensory deficits and anti-GM2 IgM antibody. CMV-infected fibroblasts express the GM2 epitope. Fisher syndrome (FS), characterised by ophthalmoplegia, ataxia, and areflexia, is a GBS variant associated with anti-GQ1b IgG antibody. GQ1b is enriched in the cranial nerves that innervate the extraocular muscles. Some patients develop FS after C jejuni infection, and the lipopolysaccharide present bears the GQ1b epitope. Molecular mimicry is a possible cause of GBS and FS.
Yuki
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Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan. yuki@dokkyomed.ac.jp
D000818:Animals; D002169:Campylobacter Infections / Q000150:complications*; D016123:Campylobacter jejuni; D002644:Chickenpox / Q000150:complications; D003586:Cytomegalovirus Infections / Q000150:complications*; D020031:Epstein-Barr Virus Infections / Q000150:complications; D005732:Gangliosides / Q000276:immunology; D020275:Guillain-Barre Syndrome / Q000209:etiology*; D014645:Herpesvirus 3, Human; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis; D019846:Miller Fisher Syndrome / Q000209:etiology; D018716:Molecular Mimicry
D005732:Gangliosides; D007074:Immunoglobulin G