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通过抑制调节T细胞的招募,CCL17会加重心肌损伤

Guoshuai Feng¹, Geetika Bajpai¹, Pan Ma¹

¹Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St Louis, MO (G.F., G.B., P.M., A.K., A.B., I.L., L.L., K.J.L.).

|February 3, 2022

概括

促进炎症细胞对心脏进行不利的重塑. 抑制CCL17增强调节性T细胞 (Treg) 招募,减少心肌炎症和改善心脏功能.

科学领域:

心血管生物学
免疫学
分子医学

背景情况:

C-C 化学因子受体2型 (CCR2) 标记了与左心室重塑和心力衰竭有关的促炎性免疫细胞.
了解CCR2+细胞介导损伤的机制对于开发治疗心肌炎症至关重要.

研究的目的:

调查C-C化学因子17 (CCL17) 在不良LV重塑和心力衰竭中的作用.
确定CCL17的细胞来源和调节途径.
确定CCL17对免疫细胞贩运和心脏功能的功能影响.

主要方法:

使用心肌梗塞,高血压和心肌细胞切除的小鼠模型.
使用Ccl17淘汰小鼠,流细胞测量,RNA测序和细胞耗尽研究.
分析了包括STAT5和NF-κB在内的信号通路,以及化学因子受体相互作用 (CCR4).

主要成果:

作为对心脏损伤的反应,CCL17由CCR2+巨细胞和树突细胞表达.
通过GM-CSF调节的CCL17信号,促进LV重塑和纤维化.
通过通过CCR4对抗CCL22介导的信号,CCL17抑制了调节性T细胞 (Treg) 的招募.
通过Treg丰度的增加,Ccl17的删除改善了心脏功能和减少了炎症.

结论:

在受伤的心脏中,CCL17起到由CCR2+细胞产生的促炎媒介作用.
向CCL17可能是一种治疗策略,可以增强Treg的注入,减轻心肌炎症和不良重塑.

关键词:

调控性T淋巴细胞化学物质 CCL17 树突细胞炎症的发生巨细胞单细胞

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