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中性粒细胞 - 微质相互作用驱动神经炎光学模型中的运动功能障碍,由亚脑骨AQP4-IgG诱导

Fangfang Qi¹, Vanda A Lennon¹, Shunyi Zhao²

¹Department of Laboratory Medicine/Pathology, Mayo Clinic, Rochester, United States of America.

The Journal of clinical investigation

|February 10, 2026

概括

中性粒细胞的招募和激活通过微质上的C5aR1信号驱动早期的光学神经炎 (NMO) 病理,在显著的组织损伤发生之前引起可逆的运动神经元功能障碍.

科学领域:

神经免疫学神经免疫学
神经病理学神经病理学

背景情况:

中性粒细胞和中性粒细胞外细胞陷 (NETs) 涉及早期神经omyelitis optica (NMO) 病原体.
中性粒细胞招募的精确机制及其在NMO进展中的作用尚未完全理解.

研究的目的:

在补充激活之前,研究在NMO小鼠模型中驱动中性粒细胞招募和致病作用的分子和细胞事件.

主要方法:

在小鼠模型中,对非补充激活的AQP4-IgG进行连续的脑下输液.
在体内两光子和电子显微镜用于细胞相互作用.
评估运动功能,血脑屏障完整性和微质/神经元变化.
基因剥离和药理上抑制C5aR1.1.
人类NMO脊髓组织的免疫组织化学分析.

主要成果:

中性粒细胞透C5a,微质激活和运动障碍发生而没有血脑屏障泄漏.
在停止AQP4-IgG输液后,运动缺陷和神经元功能障碍是可逆的.
观察到中性粒细胞与微质细胞的相互作用;切除任何一种细胞类型都能减少运动缺陷.
C5aR1缺乏或抑制减弱了中性粒细胞透,微质激活,神经元负担和运动障碍.
人类NMO病变显示了与运动神经元附近的疾病相关的微质细胞.

结论:

通过微质C5aR1传递中性细胞衍生的C5a信号是NMO中可逆运动神经元功能障碍的关键早期驱动因素.
这条途径在NMO的前细胞分解阶段运作,在经典的补体介导损伤之前.

关键词:

自身免疫性疾病是一种自身免疫性疾病.这是一种自身免疫力.神经科学是一个神经科学.

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