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SARS-CoV-2 刺突蛋白不具有固有类超抗原样炎症活性。

SARS-CoV-2 Spike Does Not Possess Intrinsic Superantigen-like Inflammatory Activity.

机构信息

Department of Biology and Biotechnology Charles Darwin, Sapienza University, 00185 Rome, Italy.

Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University, 00185 Rome, Italy.

出版信息

Cells. 2022 Aug 15;11(16):2526. doi: 10.3390/cells11162526.

DOI:10.3390/cells11162526
PMID:36010602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9406418/
Abstract

Multisystem inflammatory syndrome in children (MIS-C) is a rare hyperinflammatory disease occurring several weeks after SARS-CoV-2 infection. The clinical similarities between MIS-C and the toxic shock syndrome, together with the preferential expansion of T cells with a T-cell receptor variable β chain (TCRVβ) skewing, suggested a superantigen theory of MIS-C. For instance, recent in silico modelling evidenced the presence of a highly conserved motif within SARS-CoV-2 spike protein similar in structure to the superantigenic fragment of staphylococcal enterotoxin B (SEB). However, experimental data on the superantigenic activity of the SARS-CoV-2 spike have not yet been provided. Here, we assessed the superantigenic activity of the SARS-CoV-2 spike by analysing inflammatory cytokine production in both Jurkat cells and the peripheral blood CD4 T cells stimulated with the SARS-CoV-2 spike or SEB as a control. We found that, unlike SEB, the SARS-CoV-2 spike does not exhibit an intrinsic superantigen-like activity.

摘要

儿童多系统炎症综合征(MIS-C)是一种罕见的超炎症性疾病,发生在 SARS-CoV-2 感染后数周。MIS-C 与中毒性休克综合征之间存在临床相似性,加上 T 细胞受体可变 β 链(TCRVβ)偏向性的 T 细胞优先扩增,提示了 MIS-C 的超抗原理论。例如,最近的计算机模拟证据表明,SARS-CoV-2 刺突蛋白中存在一个高度保守的结构,类似于葡萄球菌肠毒素 B(SEB)的超抗原片段。然而,关于 SARS-CoV-2 刺突的超抗原活性的实验数据尚未提供。在这里,我们通过分析 Jurkat 细胞和外周血 CD4 T 细胞在 SARS-CoV-2 刺突或 SEB 刺激下产生的炎症细胞因子来评估 SARS-CoV-2 刺突的超抗原活性。我们发现,与 SEB 不同,SARS-CoV-2 刺突不表现出固有类似超抗原的活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4673/9406418/ee91f4c2e1bd/cells-11-02526-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4673/9406418/ee91f4c2e1bd/cells-11-02526-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4673/9406418/ee91f4c2e1bd/cells-11-02526-g001.jpg

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2
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3
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5
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