单细胞的FcγR介导的SARS-CoV-2感染激活了炎症
Caroline Junqueira1,2,3, Ângela Crespo4,5, Shahin Ranjbar4,6
1Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA. caroline.junqueira@childrens.harvard.edu.
Nature
|April 6, 2022
概括
SARS-CoV-2 感染单细胞,引发炎细胞激活和热死. 这种炎症性细胞死亡会阻止病毒的复制,但会导致COVID-19的全身炎症.
科学领域:
- 免疫学
- 病毒学
- 病变发生
背景情况:
- 严重的COVID-19与严重的炎症有关,但SARS-CoV-2引发这种反应的机制尚不清楚.
- 单细胞和巨细胞是关键的免疫细胞,参与感知病原体并通过炎症酶激活启动炎症反应.
研究的目的:
- 研究单细胞和巨细胞在SARS-CoV-2引起的炎症中的作用.
- 阐明SARS-CoV-2引发免疫细胞炎症细胞死亡的机制.
主要方法:
- 分析来自COVID-19患者的SARS-CoV-2感染单细胞.
- 通过Fcγ受体对单细胞的SARS-CoV-2抗体依赖吸收的研究.
- 在受感染的单细胞和巨细胞中评估炎细胞激活 (NLRP3,AIM2),卡斯巴-1,和气皮D.
- 检查COVID-19患者的肺部尸检组织.
主要成果:
- 大约6%的COVID-19患者的血液单细胞感染了SARS-CoV-2,这取决于抗体对病毒的吸收.
- 单细胞感染SARS-CoV-2被中止,没有产生传染性病毒.
- 受感染的单细胞经历了NLRP3和AIM2炎症酶激活,卡斯帕酶-1和加斯德明D的介导.
- 在COVID-19患者的肺部解剖样本中,在组织寄存的巨细胞中观察到激活的炎细胞.
结论:
- 单细胞和巨细胞通过抗体介导吸收SARS-CoV-2会触发炎酶激活和热死.
- 这种炎症性细胞死亡机制会阻止传染性病毒的产生,但会导致系统性炎症和COVID-19的发病.
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