BRAIN and NERVE Shinkei Kenkyu no Shinpo Volume 67, Issue 11 (November 2015)
Japanese

Autoantibodies in Guillain-Barré Syndrome Ayumi Uchibori 1 , Atsuro Chiba 1 1Department of Neurology, School of Medicine, Kyorin University Keyword: ギラン・バレー症候群 , フィッシャー症候群 , 自己抗体 , 糖脂質抗体 , ガングリオシド抗体 , Guillain-Barré syndrome , Fisher syndrome , autoantibody , anti-glycolipids antibody , anti-ganglioside antibody pp.1347-1357
Published Date 2015/11/1
DOI https://doi.org/10.11477/mf.1416200305
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Abstract

Serum antibodies against glycolipids, mainly gangliosides, are detected in about 60% of patients with Guillain-Barré syndrome (GBS) and its variants. Anti-glycolipid antibodies play a crucial role in the pathogenic mechanisms of GBS. The antibody titer is the highest in the acute phase and decreases gradually. Molecular mimicries occur between the glycolipids and surface molecules on the infectious agents. Clinical subtypes of GBS are related to the antigenic specificities of the antibodies. The distribution of gangliosides in peripheral nervous tissues could explain the different clinical manifestations. The anti-GQ1b antibody is detected in 80-90% of patients with Fisher syndrome characterized by ophthalmoplegia. GQ1b is localized in the paranodes of the human cranial nerves innervating the extraocular muscles. This is consistent with the clinical association between the anti-GQ1b antibody and ophthalmoplegia. The anti-GM1 antibody is associated with acute motor axonal neuropathy, whereas the anti-GD1b antibody is detected in acute sensory ataxic neuropathy. GBS animal models sensitized by gangliosides, such as GM1 or GD1b, develop monophasic peripheral neuropathies. In the animal models, disruption of molecule clusters and deposition of complement products were observed in the nodal and paranodal regions. Clinical and experimental data suggest complement-mediated pathogenic mechanisms triggered by anti-glycolipid antibodies in GBS.


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基本情報

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BRAIN and NERVE-神経研究の進歩
67巻11号 (2015年11月)
電子版ISSN 1344-8129 印刷版ISSN 1881-6096 医学書院

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