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肠道病毒D68型所致神经系统疾病:向免疫发病机制倾斜

EV-D68 neurological disease: tipping the scales toward immunopathogenesis.

作者信息

Krug Peter W

出版信息

J Clin Invest. 2025 Aug 1;135(15). doi: 10.1172/JCI195839.

Abstract

Over the last decade, there have been multiple outbreaks of enterovirus D68 (EV-D68) disease and associated cases of acute flaccid myelitis (AFM). The underlying cause of EV-D68-induced AFM is contentious; whether spinal cord motor neurons are damaged by direct viral infection, infiltration of immune cells, or a combination of both is not clear. In this issue of the JCI, Woods Acevedo and coworkers used a neonatal WT mouse model of EV-D68 infection to attribute paralytic disease to immune cell infiltration into the spinal cord. The results of their work in cytokine-knockout or immune cell-depleted animals effectively argue that immunopathogenesis plays an integral role in EV-D68-induced AFM.

摘要

在过去十年中,曾多次爆发肠道病毒D68(EV-D68)疾病及相关急性弛缓性脊髓炎(AFM)病例。EV-D68引发AFM的根本原因存在争议;脊髓运动神经元是被病毒直接感染、免疫细胞浸润,还是两者共同作用所损伤尚不清楚。在本期《临床研究杂志》中,伍兹·阿塞韦多及其同事利用EV-D68感染的新生野生型小鼠模型,将麻痹性疾病归因于免疫细胞浸润脊髓。他们在细胞因子敲除或免疫细胞耗竭动物身上的研究结果有力地表明,免疫发病机制在EV-D68引发的AFM中起着不可或缺的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc38/12321398/8268d2e34c76/jci-135-195839-g067.jpg

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