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Molecular mimicry between the lipooligosaccharide (LOS) component of\n                    <jats:italic>Campylobacter jejuni<\/jats:italic>\n                    and human peripheral nerve gangliosides is believed to play an important role in the pathogenesis of GBS. Conventional treatment strategies for patients with GBS include plasmapheresis, intravenous immunoglobulin (IVIG), and immunosuppression, which are invasive or relatively ineffective. In this study, we used our animal model of GBS, in which Lewis rats were immunized with GD3\u2010like LOS isolated from\n                    <jats:italic>C.jejuni<\/jats:italic>\n                    . The animals developed anti\u2010GD3 ganglioside antibodies and manifested neuromuscular dysfunction. To develop novel therapeutic strategies, we treated the animals by intraperitoneal administration of an anti\u2010GD3 antiidiotype monoclonal antibody (BEC2) that specifically interacts with the pathogenic antibody. The treated animals had a remarkable reduction of anti\u2010GD3 antibody titers and improvement of motor nerve functions. The results suggest that ganglioside mimics, such as antiidiotype antibodies, may be powerful reagents for therapeutic intervention in GBS by neutralizing specific pathogenic antiganglioside antibodies. \u00a9 2010 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jnr.22330","type":"journal-article","created":{"date-parts":[[2010,1,13]],"date-time":"2010-01-13T11:43:45Z","timestamp":1263383025000},"page":"1651-1663","source":"Crossref","is-referenced-by-count":21,"title":["Novel anti\u2010idiotype antibody therapy for lipooligosaccharide\u2010induced experimental autoimmune neuritis: Use relevant to Guillain\u2010Barr\u00e9 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