title: [Pathogenesis of axonal Guillain-Barré syndrome].
abstract: We identified IgG antibody to GM1 ganglioside in patients with axonal Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis, and that there is molecular mimicry between GM 1 and the bacterial lipooligosaccharide. On sensitization with GM1 as well as C. jejuni lipo-oligosaccharide, rabbits developed anti-GM1 IgG antibody and flaccid limb weakness. Paralyzed rabbits had pathological changes in their peripheral nerves identical to those present in axonal Guillain-Barré syndrome. These findings show that molecular mimicry is an important cause of Guillain-Barr6 syndrome. This new concept that carbohydrate mimicry can cause an autoimmune disease provides a clue to the resolution of the pathogenesis of other immune-mediated diseases.
authors.affiliation: Department of Neurology and Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Yuki
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000032:analysis*; D002169:Campylobacter Infections / Q000150:complications; D016123:Campylobacter jejuni; D005677:G(M1) Ganglioside / Q000276:immunology*; D020275:Guillain-Barre Syndrome / Q000209:etiology* / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D008070:Lipopolysaccharides / Q000737:chemistry; D018716:Molecular Mimicry; D011817:Rabbits
chemical_list: D001323:Autoantibodies; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D005677:G(M1) Ganglioside