在SARS-CoV-2肺炎中感染的巨细胞和T细胞之间的循环
Rogan A Grant1, Luisa Morales-Nebreda1, Nikolay S Markov1
1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Nature
|January 11, 2021
概括
严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 引发肺部持续的免疫反应. 膜巨细胞和T细胞形成反循环,导致严重的COVID-19肺炎持续炎症.
科学领域:
- 免疫学
- 病毒学
- 肺病学
背景情况:
- 严重急性呼吸综合征冠状病毒2 (SARS-CoV-2) 可能导致严重的肺炎和急性呼吸应急综合征 (ARDS).
- 在SARS-CoV-2感染期间,气泡内的特定免疫反应尚未完全理解,可能与其他肺炎不同.
研究的目的:
- 通过描述感染患者气泡中的免疫反应来调查SARS-CoV-2的病理生物学.
- 将SARS-CoV-2感染的气膜免疫环境与其他肺炎进行比较.
主要方法:
- 收集了88名SARS-CoV-2呼吸衰竭患者和211名其他肺炎患者的支气管洗液.
- 使用流细胞测量和批量转录基因分析.
- 在输管后48小时内对重症COVID-19患者的样本进行单细胞RNA测序.
主要成果:
- 大多数SARS-CoV-2感染患者的气泡空间显示T细胞和单细胞持续丰富.
- 转录基因分析表明,SARS-CoV-2 感染了气膜巨细胞,导致T细胞化学吸引剂的产生.
- 通过干扰素-γ 和细胞因子释放,发现了 SARS-CoV-2 感染的膜巨细胞和 T 细胞促进持续的膜炎症的正反循环.
结论:
- SARS-CoV-2 感染会引起一种独特的,缓慢发展的局部性气泡炎.
- 在严重的COVID-19期间,T细胞和膜巨细胞相互作用的循环会导致膜持续炎症.
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