Intense immunological dysregulation including immune cell lesions has been characteristically observed in severe cases of coronavirus disease-2019 (COVID-19), for which molecular mechanisms are not properly understood. A study of physiological expressions of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) host cell entry-related factors in immune system components may help explain molecular mechanisms involved in COVID-19 immunopathology. We analyzed transcriptomic and proteomic expression metadata for SARS-CoV-2 host cell entry receptor ACE2 and entry associated proteases (TMPRSS2, CTSL, and FURIN) in silico across immune system components including the blood lineage cells. ACE2 was not detected in any of the studied immune cell components; however, varying transcriptomic and proteomic expressions were observed for TMPRSS2, CTSL, and FURIN. Nondetectable expressions of SARS-CoV-2 host cell entry receptor ACE2 in immune system components or blood lineage cells indicate it does not mediate immune cell lesions in COVID-19. Alternative mechanisms need to be explored for COVID-19 immunopathogenesis.

中文翻译：

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SARS-CoV-2宿主细胞进入因子在健康个体免疫系统成分中的表达及其与COVID-19免疫病理学的相关性

在严重的冠状病毒病 2019 (COVID-19) 病例中，特征性地观察到了包括免疫细胞病变在内的严重免疫失调，其分子机制尚不清楚。对免疫系统成分中严重急性呼吸系统综合症冠状病毒-2 (SARS-CoV-2) 宿主细胞进入相关因子的生理表达的研究可能有助于解释 COVID-19 免疫病理学的分子机制。我们分析了SARS-CoV的-2进入宿主细胞的受体转录和蛋白质组表达的元数据ACE2和条目相关联的蛋白酶（TMPRSS2，CTSL，和弗林蛋白酶），在硅片整个免疫系统组件，包括血细胞谱系细胞。ACE2在任何研究的免疫细胞成分中均未检测到；然而，对TMPRSS2、CTSL和FURIN观察到了不同的转录组和蛋白质组表达。SARS-CoV-2 宿主细胞进入受体ACE2在免疫系统成分或血系细胞中检测不到的表达表明它不会介导 COVID-19 中的免疫细胞病变。需要探索 COVID-19 免疫发病机制的替代机制。