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自身免疫性突触病。

Autoimmune synaptopathies.

机构信息

UCL Institute of Neurology, University College London, Queen Square House, Queen Square, London WC1N 3BG, UK.

Nuffield Department of Clinical Neurosciences, University of Oxford, Level 6, West Wing, John Radcliffe Hospital, Oxford OX3 9DU, UK.

出版信息

Nat Rev Neurosci. 2016 Feb;17(2):103-17. doi: 10.1038/nrn.2015.27.

Abstract

Autoantibodies targeting proteins at the neuromuscular junction are known to cause several distinct myasthenic syndromes. Recently, autoantibodies targeting neurotransmitter receptors and associated proteins have also emerged as a cause of severe, but potentially treatable, diseases of the CNS. Here, we review the clinical evidence as well as in vitro and in vivo experimental evidence that autoantibodies account for myasthenic syndromes and autoimmune disorders of the CNS by disrupting the functional or structural integrity of synapses. Studying neurological and psychiatric diseases of autoimmune origin may provide new insights into the cellular and circuit mechanisms underlying a broad range of CNS disorders.

摘要

针对神经肌肉接头处蛋白的自身抗体已被证实可引起多种不同的肌无力综合征。最近,针对神经递质受体和相关蛋白的自身抗体也被认为是导致中枢神经系统严重但潜在可治疗疾病的原因。在这里,我们综述了临床证据以及体外和体内实验证据,这些证据表明自身抗体通过破坏突触的功能或结构完整性而导致肌无力综合征和中枢神经系统自身免疫性疾病。研究自身免疫性起源的神经和精神疾病可能为广泛的中枢神经系统疾病的细胞和回路机制提供新的见解。

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