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通过调节巨细胞极化和中性细胞透,Dectin-1 促进心肌缺血/再输损伤
Qin Fan1,2, Rong Tao1, Hang Zhang1,2
1Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China.
Circulation
|December 28, 2018
概括
通过促进炎症和免疫细胞透,Dectin-1 在心肌缺血/反损伤中起着关键作用. 抑制Dectin-1可以改善心脏功能,并为心脏病发作恢复提供潜在的治疗点.
科学领域:
- 免疫学
- 心脏病学
- 分子生物学
背景情况:
- 在心肌缺血/反 (IR) 损伤中,与巨相关的免疫反应至关重要.
- 骨髓细胞上的模式识别受体Dectin-1调节免疫平衡,但其在心肌红外损伤中的作用尚不清楚.
研究的目的:
- 调查Dectin-1在心肌内射损伤中的功能意义.
- 探索Dectin-1作为心肌红外损伤的潜在治疗点.
主要方法:
- 在小鼠中利用基因切除,抗体阻断和Dectin-1激活模型.
- 使用流细胞测量,qPCR和免疫组织化学分析免疫细胞透和炎症.
- 在ST段升高心肌梗塞患者中评估Dectin-1+细胞水平.
主要成果:
- 在心脏IR损伤后的巨细胞上增加了dectin-1表达.
- 德-1 缺乏改善了心脏功能,减少了细胞亡,减少了M1 巨细胞的偏离和免疫细胞的透.
- 德1通过Cxcl1和G-CSF促进了中性粒细胞的招募,而IL-23/IL-1β的产生对γδT细胞的IL-17A表达至关重要.
- 在心肌梗塞患者中观察到循环Dectin-1+单细胞水平升高,与心脏功能障碍相关.
结论:
- 德1在心肌红外损伤中起着至关重要的作用.
- 针对Dectin-1是一种有前途的治疗策略.
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