Pathogenesis of axonal Guillain-Barré syndrome

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.