神经脊髓炎中的少突胶质细胞。

Q3 Neuroscience
Ai Guo, Yuzhen Wei, Alexei Verkhratsky, Fu-Dong Shi
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引用次数: 0

摘要

视神经脊髓炎谱系障碍(NMOSD)是一种中枢神经系统炎症性自身免疫性疾病,其水通道蛋白-4免疫球蛋白G (AQP4- igg)靶向定位于星形细胞终足的水通道水通道蛋白-4 (AQP4),从而引发炎症病变和组织损伤。NMOSD的病理特征是少突胶质细胞早期缺失、广泛脱髓鞘和轴突损伤。NMOSD少突胶质细胞损伤的发病机制包括补体依赖性旁观者效应、抗体依赖性细胞介导的细胞毒性旁观者效应、谷氨酸毒性、连接蛋白失调和血脑屏障破坏。急性NMOSD病变的再髓鞘水平较低。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oligodendroglia in Neuromyelitis Optica Spectrum Disorder.

Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the central nervous system, in which aquaporin-4 immunoglobulin G (AQP4-IgG) targets the water channel aquaporin-4 (AQP4) localized at astrocytic endfeet, thus triggering inflammatory lesions and tissue damage. The pathological characteristics of NMOSD are early loss of oligodendrocytes, extensive demyelination, and axonal injury. The pathogenesis of oligodendrocyte damage in NMOSD includes complement-dependent bystander effect, antibody-dependent cell-mediated cytotoxicity bystander effect, glutamate toxicity, connexin dysregulation, and blood-brain barrier disruption. Remyelination levels in acute NMOSD lesions are low.

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来源期刊
Advances in neurobiology
Advances in neurobiology Neuroscience-Neurology
CiteScore
2.80
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0.00%
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