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Antibodies against gangliosides and ganglioside complexes in Guillain-Barre syndrome: New aspects of research

机译:Guillain-Barre综合征中针对神经节苷脂和神经节苷脂复合物的抗体:研究的新方面

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Guillain-Barre syndrome (GBS) is an acute autoimmune neuropathy, often preceded by an infection. Serum anti-ganglioside antibodies are frequently elevated in titer. Those antibodies are useful for diagnosis. Some of them also may be directly involved in the pathogenetic mechanisms by binding to the regions where the respective target ganglioside is specifically localized. We have recently found the presence of the antibody that specifically recognizes a new conformational epitope formed by two gangliosides (ganglioside complex) in the acute-phase sera of some GBS patients. In particular, the antibodies against GD1a/GD1b and/or GD1b/GT1b complexes are associated with severe GBS requiring artificial ventilation. Some patients with Miller Fisher syndrome also have antibodies against ganglioside complexes including GQ1b; such as GQ1b/GM1 and GQ1b/GD1a. Gangliosides along with other components as cholesterol are known to form lipid rafts, in which the carbohydrate portions of two different gangliosides may form a new conformational epitope. Within the rafts, gangliosides are considered to interact with important receptors or signal transducers. The antibodies against ganglioside complexes may therefore directly cause nerve conduction failure and severe disability in GBS. More study is needed to elucidate the roles of the antibodies against ganglioside complexes. (c) 2007 Elsevier B.V. All rights reserved.
机译:格林巴利综合征(GBS)是一种急性自身免疫性神经病,通常在感染之前。血清抗神经节苷脂抗体的滴度经常升高。这些抗体可用于诊断。它们中的一些还可以通过结合到各个靶神经节苷脂被专门定位的区域而直接参与致病机制。我们最近发现在某些GBS患者的急性期血清中存在特异性识别由两个神经节苷脂(神经节苷脂复合物)形成的新构象表位的抗体。特别地,针对GD1a / GD1b和/或GD1b / GT1b复合物的抗体与需要人工通气的严重GBS有关。一些患有Miller Fisher综合征的患者也具有针对神经节苷脂复合物(包括GQ1b)的抗体。例如GQ1b / GM1和GQ1b / GD1a。已知神经节苷脂与其他成分(如胆固醇)会形成脂质筏,其中两个不同神经节苷脂的碳水化合物部分可能会形成新的构象表位。在木筏中,神经节苷脂被认为与重要的受体或信号传感器相互作用。因此,针对神经节苷脂复合物的抗体可能直接导致GBS中的神经传导衰竭和严重残疾。需要更多的研究来阐明抗神经节苷脂复合物的抗体的作用。 (c)2007 Elsevier B.V.保留所有权利。

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