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单细胞RNA测序以剖析自身免疫性心肌炎的免疫网络

Xiumeng Hua¹, Gang Hu², Qingtao Hu³

¹State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (X.H., Y.C., Y.H., X.C., J.S.).

|May 21, 2020

概括

这项研究揭示了实验性自身免疫性心肌炎 (EAM) 中的免疫细胞网络,并确定HIF1A是心脏炎症的关键调节者. 针对HIF1A可能为心肌炎和相关心脏病提供新的治疗策略.

科学领域:

免疫学
心脏病学
分子生物学

背景情况:

心肌炎可能发展为扩张性心肌病, 这种情况可能需要心脏移植.
目前尚不完全了解肌心炎进展的免疫机制.
识别炎症反应中的关键基因对于了解疾病的发病过程至关重要.

研究的目的:

在从心肌炎过渡到心肌病期间调查免疫网络.
鉴定导致心肌炎炎症反应的基因.
探索HIF1A在心脏炎症中的作用及其治疗潜力.

主要方法:

在小鼠中使用肌重链α生成了一种实验性自身免疫心肌炎 (EAM) 模型.
在不同EAM阶段对心脏免疫细胞 (Cd45+) 进行单细胞RNA测序.
分析了心脏移植患者的心脏组织.

主要成果:

在整个EAM阶段,巨细胞是主要的免疫细胞 (> 60%),与炎症相关的群体显示上调的HIF1A调节基因.
中性粒细胞在EAM诱导后增加,释放IL-1;T细胞在亚急性阶段达到峰值.
分别显示了HIF1A调节的基因和IL-17释放;HIF1A表达与炎症程度相关.
在EAM模型中,PX-478是一种HIF1A抑制剂,可缓解炎症反应.
与扩大心肌病和健康对照人群相比,HIF1A在人类急性自身免疫心肌炎中升高.

结论:

在EAM中建立了心脏细胞的综合单细胞免疫格局.
通过调节巨细胞群2和T辅助细胞活动,HIF1A对炎症反应有显著的作用.
在EAM模型中,通过减少炎症细胞透,HIF1A抑制显示出治疗潜力,这表明它是临床点.

关键词:

人类HIF1A蛋白炎症的发生心肌炎治疗药物转录组

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