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免疫受体SLAMF5调节了多发性硬化症中髓状细胞介导的神经炎症

Laura Bellassen¹, Keren David¹, Bar Lampert¹

¹Department of Systems Immunology, Weizmann Institute of Science, Rehovot, Israel.

|September 8, 2025

概括

SLAMF5阻断减少了多发性硬化症 (MS) 中的髓状细胞激活. 这针对神经炎症,为MS和其他自身免疫性疾病提供了潜在的治疗策略.

科学领域:

神经免疫学神经免疫学
细胞和分子免疫学细胞和分子免疫学
自免疫性疾病自免疫性疾病

背景情况:

多发性硬化症 (MS) 涉及到由髓状细胞驱动的中枢神经系统 (CNS) 脱髓化和神经炎症.
微细胞和巨细胞是MS病变的关键参与者,调节炎症反应.
细胞表面受体SLAMF5通过粘附和信号调节免疫细胞活动.

研究的目的:

调查SLAMF5在中枢神经系统内髓状细胞激活中的作用,在实验性自身免疫脑膜炎 (EAE) 期间,MS的小鼠模型.
探索SLAMF5作为MS的潜在治疗点.

主要方法:

利用鼠类MS模型 (EAE) 研究SLAMF5在髓状细胞中的功能.
研究了SLAMF5缺乏和药物阻断对免疫细胞激活标记物的影响 (MHCII,CD80,CD52).
在人类外围单细胞和iPSC衍生的微质细胞中分析了SLAMF5阻塞.

主要成果:

骨髓细胞中的SLAMF5缺乏减少了MHCII和CD80的表达,由BHLHE40和CD52介导.
这种缺陷延迟了EAE的发病,并减少了疾病的进展.
药理学上的SLAMF5阻断阻止了EAE的进展,并降低了髓状细胞激活标志物.
阻塞降低了HLA-DR,CD80和CD52在人类MS单细胞和微质细胞中的表达.

结论:

SLAMF5是神经炎症中髓状细胞激活的关键调节者.
准SLAMF5为MS和其他自身免疫性疾病提供了一个有希望的治疗途径.

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