遇见数据集

Dataset related to article "Recognition and inhibition of SARS-CoV-2 by humoral innate immunity pattern recognition molecules"

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Zenodo2023-01-02 更新2026-05-26 收录
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This record contains raw data related to article “Recognition and inhibition of SARS-CoV-2 by humoral innate immunity pattern recognition molecules" The humoral arm of innate immunity includes diverse molecules with antibody-like functions, some of which serve as disease severity biomarkers in coronavirus disease 2019 (COVID-19). The present study was designed to conduct a systematic investigation of the interaction of human humoral fluid-phase pattern recognition molecules (PRMs) with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Of 12 PRMs tested, the long pentraxin 3 (PTX3) and mannose-binding lectin (MBL) bound the viral nucleocapsid and spike proteins, respectively. MBL bound trimeric spike protein, including that of variants of concern (VoC), in a glycan-dependent manner and inhibited SARS-CoV-2 in three in vitro models. Moreover, after binding to spike protein, MBL activated the lectin pathway of complement activation. Based on retention of glycosylation sites and modeling, MBL was predicted to recognize the Omicron VoC. Genetic polymorphisms at the MBL2 locus were associated with disease severity. These results suggest that selected humoral fluid-phase PRMs can play an important role in resistance to, and pathogenesis of, COVID-19, a finding with translational implications.

本数据集包含与论文《体液固有免疫模式识别分子识别并抑制新型冠状病毒(SARS-CoV-2)》相关的原始研究数据。体液固有免疫系统包含多种具备抗体样功能的分子,其中部分分子可作为新型冠状病毒肺炎(COVID-19)的疾病严重程度生物标志物。本研究旨在系统性探究人类体液液相模式识别分子(pattern recognition molecules, PRMs)与严重急性呼吸综合征冠状病毒2(SARS-CoV-2)的相互作用。在本次测试的12种PRMs中,长正五聚蛋白3(long pentraxin 3, PTX3)与甘露聚糖结合凝集素(mannose-binding lectin, MBL)分别结合病毒核衣壳蛋白与刺突蛋白。MBL以糖基依赖的方式结合三聚体刺突蛋白(包括当前关切变异株(variants of concern, VoC)的刺突蛋白),并在三种体外模型中抑制SARS-CoV-2。此外,MBL结合刺突蛋白后可激活补体系统的凝集素途径。基于糖基化位点保守性与结构建模分析,MBL被预测可识别奥密克戎关切变异株(Omicron VoC)。MBL2基因座的遗传多态性与疾病严重程度显著相关。上述研究结果表明,特定的体液液相PRMs可在新型冠状病毒肺炎的宿主防御与发病进程中发挥关键作用,该发现具备重要的转化研究价值。

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2023-01-02
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