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首页> 外文期刊>The European Journal of Neuroscience >Neuronal central nervous system syndromes probably mediated by autoantibodies
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Neuronal central nervous system syndromes probably mediated by autoantibodies

机译：自身抗体介导的神经元中枢神经系统综合征

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摘要

In the last few years, a rapidly growing number of autoantibodies targeting neuronal cell-surface antigens have been identified in patients presenting with neurological symptoms. Targeted antigens include ionotropic receptors such as N-methyl-d-aspartate receptor or the -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor, metabotropic receptors such as mGluR1 and mGluR5, and other synaptic proteins, some of them belonging to the voltage-gated potassium channel complex. Importantly, the cell-surface location of these antigens makes them vulnerable to direct antibody-mediated modulation. Some of these autoantibodies, generally targeting ionotropic channels or their partner proteins, define clinical syndromes resembling models of pharmacological or genetic disruption of the corresponding antigen, suggesting a direct pathogenic role of the associated autoantibodies. Moreover, the associated neurological symptoms are usually immunotherapy-responsive, further arguing for a pathogenic effect of the antibodies. Some studies have shown that some patients' antibodies may have structural and functional invitro effects on the targeted antigens. Definite proof of the pathogenicity of these autoantibodies has been obtained for just a few through passive transfer experiments in animal models. In this review we present existing and converging evidence suggesting a pathogenic role of some autoantibodies directed against neuronal cell-surface antigens observed in patients with central nervous system disorders. We describe the main clinical symptoms characterizing the patients and discuss conflicting arguments regarding the pathogenicity of these antibodies.
机译：在过去的几年中，已经在出现神经系统症状的患者中发现了迅速增长的针对神经元细胞表面抗原的自身抗体。靶向抗原包括离子型受体，例如N-甲基-d-天冬氨酸受体或-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体，代谢型受体，例如mGluR1和mGluR5，以及其他突触蛋白，其中一些属于电压门控钾通道复合物。重要的是，这些抗原在细胞表面的位置使其容易受到抗体介导的直接调节的影响。这些自身抗体中的一些通常靶向离子性通道或其伴侣蛋白，定义了类似于相应抗原的药理或遗传破坏模型的临床综合征，表明相关自身抗体的直接致病作用。而且，相关的神经系统症状通常是免疫治疗反应性的，进一步证明了抗体的致病作用。一些研究表明，某些患者的抗体可能对靶向抗原具有结构和功能的体外作用。这些自身抗体的致病性的确凿证据仅通过动物模型中的被动转移实验获得了少数。在这篇综述中，我们提供了现有的和越来越多的证据，这些证据表明某些针对中枢神经系统疾病患者中观察到的神经元细胞表面抗原的自身抗体的致病作用。我们描述了表征患者特征的主要临床症状，并讨论了有关这些抗体的致病性的相互矛盾的论点。

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