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I型IFN减少SARS-CoV-2在人类心肌细胞中的复制,并增加巨细胞中细胞因子的生产

Verónica Durán^1,2,3, Eirini Nikolouli⁴, Shambhabi Chatterjee^5,6

¹Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research [HZI], Braunschweig, and the Hannover Medical School [MHH], 30625, Hannover, Germany.

Journal of clinical immunology

|October 21, 2025

概括

I型干扰素减少了人心细胞中的SARS-CoV-2复制,但增强了巨细胞的炎症反应. 这一发现澄清了干扰素免疫在COVID-19严重性中的作用.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
干细胞生物学干细胞生物学

背景情况:

I型干扰素 (IFN) 免疫在COVID-19严重性中的作用尚未完全理解.
在患有IFN缺陷的患者中,对SARS-CoV-2的细胞反应的调查至关重要.

研究的目的:

阐明1型IFN缺乏症患者COVID-19严重程度的细胞机制.
分析来自IFNAR1合格和缺陷iPSCs的心肌细胞和巨细胞中的SARS-CoV-2复制和细胞因子生产.

主要方法:

从IFNAR1有能力 (IFNAR1^comp) 和缺乏 (IFNAR1^def) 诱导的多能干细胞 (iPSC) 中分化的心肌细胞和巨细胞.
暴露于SARS-CoV-2的分化细胞来分析病毒复制和细胞因子的产生.
评估了外源IFNα治疗对受感染细胞的影响.

主要成果:

心肌细胞表达ACE2并支持高SARS-CoV-2复制,在IFNAR1^def细胞中恶化.
外源IFNα在IFNAR1^comp心肌细胞中减轻了感染,但在IFNAR1^def细胞中没有.
巨细胞不支持SARS-CoV-2复制,但产生了促炎性细胞因子;这种反应在IFNAR1巨细胞中受损.

结论:

第一种类型的IFN具有双重作用:它们降低了人类iPSC衍生的心肌细胞中的SARS-CoV-2复制.
第一种类型的IFN增强了巨细胞中的细胞因子反应,导致炎症.

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