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S100A9作为神经髓炎光学谱系障碍的潜在新目标

Fei Wu¹, Xinming Rang¹, Yinglian Zhou¹

¹Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.

Multiple sclerosis and related disorders

|September 21, 2025

概括

神经脊髓炎光学谱系障碍 (NMOSD) 涉及单细胞和S100A9的神经炎症. 升高的S100A9促进M1巨细胞两极分化,驱动NMOSD病原体,并建议它作为治疗点.

科学领域:

神经免疫学神经免疫学
自免疫性疾病自免疫性疾病
中枢神经系统疾病中枢神经系统疾病

背景情况:

神经脊髓炎光学谱系障碍 (NMOSD) 是一种自身免疫性中枢神经系统疾病,主要通过aquaporin-4 (AQP4) 自体抗体向视神经和脊髓.
天生的免疫细胞,特别是单细胞/巨细胞,通过启动炎症并促进脱髓化,在NMOSD病原发生中起着至关重要的作用.

研究的目的:

调查先天性免疫细胞的作用,并确定参与NMOSD病变发生的关键基因.
探索S100A9作为NMOSD的潜在治疗标和生物标志物.

主要方法:

RNA测序 (RNA-seq) 和生物信息学分析以识别差异表达基因 (DEG) 和枢纽基因.
免疫透分析,蛋白与蛋白相互作用 (PPI) 网络分析和基因组丰富分析 (GSEA).
在NMOSD患者样本中对S100A9表达和功能测定进行实验验证.

主要成果:

RNA-seq在NMOSD中发现了326个DEG,其中单细胞的透率最高.
S100A9成为一个关键的枢纽基因,在NMOSD患者中显著升高.
细胞外S100A9通过TLR4/MyD88/NF-κB通路促进了M1巨细胞的极化,增殖和炎症因子的产生.

结论:

通过调节巨细胞功能,S100A9是NMOSD中神经炎症的关键调解者.
S100A9代表了一个潜在的诊断标记物和NMOSD的治疗点.
这项研究为NMOSD发展和进展背后的分子机制提供了新的见解.

关键词:

生物信息学分析神经炎症是一种神经炎症.在RNA-seqqq.在S100A9A9中使用.这就是THP-1的特点.通过TLR4/MyD88/NF-κB通路进行.

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