Opsonizing antibodies mediated SARS-CoV-2 entry into monocytes leads to inflammation.
Opsonizing antibodies mediated SARS-CoV-2 entry into monocytes leads to inflammation.
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调理抗体介导 SARS-CoV-2 进入单核细胞导致炎症
DOI：
10.1002/mef2.11
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发表时间：
2022-06
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Caroline Junqueira等人最近在Nature上发表的一篇论文。（2022）1揭示FcγR和调理抗体可介导严重急性呼吸综合征冠状病毒2 SARS-冠状病毒-2（SARS-CoV-2）感染单核细胞/巨噬细胞，然后激活NLRP 3炎性体、caspase-1和Gasdermin D（GSDMD），从而引发焦亡和严重的炎症反应。自2019年底首次描述以来，冠状病毒病2019由RS-CoV-2引起的COVID-19已成为最重大的全球公共卫生危机之一。在某些患者中，SARS-CoV-2感染可诱导严重的炎症细胞因子风暴，可导致呼吸综合征和多器官衰竭。1，2从生物学的角度来看，当骨髓细胞感觉到侵入性感染时，它们激活炎性小体，其招募含有半胱天冬酶招募结构域（ASC）衔接子的凋亡斑点蛋白，并进一步激活下游半胱天冬酶-1，其切割抑制剂C-结构域并释放
A recent paper published in Nature by Caroline Junqueira et al.(2022) 1 reveals that FcγR and opsonizing antibodies can mediate severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection of monocytes/macrophages, which can then activate NLRP3 inflammasomes, caspase‐1, and Gasdermin D (GSDMD), and thereby trigger pyroptosis and severe inflammatory reaction.Since the first description in late 2019, coronavirus disease 2019 (COVID‐19), caused by RS‐CoV‐2, has emerged as one of the most significant global public health crises. In some patients, SARS‐CoV‐2 infection can induce a severe inflammatory cytokine storm that can lead to respiratory syndrome and multiorgan failure. 1, 2 From a biological perspective, when myeloid cells sense invasive infection, they activate inflammasomes, which recruit apoptotic speck protein containing a caspase recruitment domain (ASC) adaptors and further activate downstream caspase‐1, which cleaves the suppressant C‐domain and releases