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Guillain\u2010Barr\u00e9 syndrome, the most frequent cause of acute neuromuscular paralysis, sometimes occurs after <jats:italic>Campylobacter jejuni<\/jats:italic> enteritis. Gangliosides are predominantly cell\u2010surface glycolipids highly expressed in nervous tissue, whilst lipo\u2010oligosaccharides are major components of the Gram\u2010negative bacterium <jats:italic>C. jejuni<\/jats:italic> outer membrane. IgG autoantibodies to GM1 ganglioside were found in the sera from patients with Guillain\u2010Barr\u00e9 syndrome. Molecular mimicry was demonstrated between GM1 and lipo\u2010oligosaccharide of <jats:italic>C. jejuni<\/jats:italic> isolated from the patients. Disease models by sensitization of rabbits with GM1 and <jats:italic>C. jejuni<\/jats:italic> lipo\u2010oligosaccharide were established. Guillain\u2010Barr\u00e9 syndrome provided the first verification that an autoimmune disease is triggered by molecular mimicry. Its disease models are helpful to further understand the molecular pathogenesis as well as to develop new treatments in Guillain\u2010Barr\u00e9 syndrome.<\/jats:p>","DOI":"10.1155\/2011\/829129","type":"journal-article","created":{"date-parts":[[2010,12,15]],"date-time":"2010-12-15T19:50:49Z","timestamp":1292442649000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":64,"title":["Guillain\u2010Barr\u00e9 Syndrome Animal Model: The First Proof of Molecular Mimicry in Human Autoimmune 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