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PP4调节巨细胞与中性粒细胞的交叉交互,以限制CCL5驱动的败血症NETosis

Feng-Ming Yang¹, Shih-Chang Hsu², Yu-Chih Wu³

¹Graduate Institute of Physiology, National Taiwan University College of Medicine, Taipei, Taiwan.

|February 22, 2026

概括

骨髓细胞中的蛋白质酸酶4 (PP4) 缺乏通过调节巨细胞与中性粒细胞交叉的失调而加剧败血症. PP4的损失通过CCL5/CCR5信号促进了过度的NETosis,突出了PP4作为败血症治疗目标.

科学领域:

免疫学免疫学免疫学
分子生物学分子生物学
病理生理学病理生理学

背景情况:

败血症是一种危及生命的疾病,其特点是过度炎症和多器官衰竭.
在致命的人类败血症中观察到骨髓细胞蛋白酸酶4 (PP4) 表达的减少.
在败血症期间,PP4在巨细胞与中性粒细胞相互作用中的特定作用尚不清楚.

研究的目的:

研究PP4在败血症期间调节先天免疫力的细胞类型特异性功能.
阐明PP4在败血症模型中影响巨细胞-中性粒细胞交叉声的分子机制.

主要方法:

产生的骨髓细胞特异性PP4淘汰小鼠.
诱导性败血症使用结和刺穿 (CLP) 和内毒素挑战.
分析了中性粒细胞的激活,NETosis,ROS的产生,以及信号通路 (CCL5/CCR5,TBK1/IRF3,ERK1/2).

主要成果:

缺乏PP4的小鼠表现出增加的败血症易感性和严重的组织损伤.
PP4的丧失导致了CCL5/CCR5信号失调,增强了中性粒细胞激活和NETosis.
PP4直接去化了TBK1,抑制了CCL5的产生;ERK1/2调节了中性粒细胞中CCR5的上调.

结论:

PP4是巨细胞-中性粒细胞交叉和败血症中NETosis的关键调节者.
CCL5/CCR5信号通路是PP4保护作用的关键媒介.
准PP4或CCL5/CCR5通路为败血症提供了一个潜在的治疗策略.

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