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通过通过TLR4/NF-κB信号通路影响微质炎症,S100A4促进实验性自身免疫脑膜炎

He Jingjing¹, Wu Tongqian², Yan Shirong³

¹Center for Clinical Laboratories, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China; Department of Clinical Laboratory, Guizhou Hospital, the First Affiliated Hospital of Sun Yat-sen University, Guiyang 550004, China.

International immunopharmacology

|September 6, 2024

概括

结合蛋白S100A4通过促进微质活化和神经元损伤,加剧了多发性硬化 (MS) 中的神经炎症. 针对S100A4可能为MS治疗提供治疗策略.

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
细胞生物学细胞生物学

背景情况:

多发性硬化症 (MS) 是一种衰弱的自身免疫性疾病,影响中枢神经系统.
结合蛋白S100A4在MS病变发生过程中的作用尚未完全理解.
微质细胞,大脑的常驻免疫细胞,在神经炎症中起着至关重要的作用.

研究的目的:

研究S100A4调节MS中神经炎症的精确机制.
确定S100A4对微质炎症的影响及其对神经元细胞的影响.
评估S100A4作为MS的潜在治疗标.

主要方法:

在体外研究中,使用S100A4淘汰BV2微质细胞.
在体内研究使用S100A4淘汰赛小鼠在MS的实验性自身免疫脑膜炎 (EAE) 模型中.
评估临床评分,炎症细胞透,脱髓化,细胞因子水平和免疫细胞频率.
对TLR4/NF-κB信号通路的研究.

主要成果:

S100A4淘汰赛小鼠显示EAE临床评分有所改善,神经炎症减少,包括较少的炎症细胞透和脱髓化.
S100A4淘汰赛小鼠在中枢神经系统和脏中表现出较低水平的炎症性细胞因子.
发现S100A4促进微质炎症,影响微质两极分化,并通过TLR4/NF-κB通路增强微质介导的神经细胞亡.

结论:

在MS中,S100A4在调节神经炎症方面发挥着重要作用,至少部分是通过调节微质炎症.
准S100A4可能代表着一种新的治疗策略,用于管理MS.
对S100A4-微质轴的进一步研究对于MS治疗的发展是有必要的.

关键词:

这是一种自身免疫力.实验性自身免疫性脑膜炎微质细胞中的微质细胞多发性硬化症是多发性硬化症.神经炎症是一种神经炎症.在 S100A4 中使用.

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