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FcγRIIa介导的严重急性呼吸综合征冠状病毒2抗体依赖性摄取增强单核细胞白细胞介素-6表达。

FcγRIIa-mediated antibody-dependent uptake of SARS-CoV-2 enhances IL-6 expression of monocytes.

作者信息

Mese Kemal, Maguilla Rosado Esther, Lüder Carsten G K, Abdel-Moneim Ahmed Sayed, Jordan Patrick, Schwanbeck Julian, Bunz Oskar, Lugert Raimond, Bohne Wolfgang, Gao Jian, Dudakova Anna, Groß Uwe, Zautner Andreas E

机构信息

1Institute for Medical Microbiology and Virology, University Medical Center Göttingen, 37075 Göttingen, Germany.

5Recent address: Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany.

出版信息

Eur J Microbiol Immunol (Bp). 2024 Dec 16;14(4):380-391. doi: 10.1556/1886.2024.00109. Print 2024 Dec 18.

DOI:10.1556/1886.2024.00109
PMID:39680053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11836651/
Abstract

This work aimed to investigate interactions between antibody-opsonized SARS-CoV-2 and monocytes enriched from human peripheral blood mononuclear cells (PBMC) to determine whether antibody dependent enhancement might contribute to the pathophysiology of COVID-19. Pre-incubation of SARS-CoV-2 with sera from hospitalized COVID-19 patients led to significantly increased virus uptake and viral replication in monocytes. Remarkably, SARS-CoV-2 pre-incubated with sera from patients with severe COVID-19 but not those with mild disease or post vaccination strongly increased IL-6 secretion by monocytes. Antibody dependent viral uptake was partially inhibited by monoclonal anti-FcγRIIa antibody whereas IL-6 secretion was completely abolished. FcγRIIa preferentially binds IgG2, and sera from patients with severe COVID-19 contained lower IgG2 levels as compared to mild COVID-19 cases whereas IgG1 levels were increased. These data suggests that FcγRIIa-mediated binding of antibody-opsonized SARS-CoV-2 critically impacts monocytic inflammatory cytokine release and COVID-19 pathophysiology.

摘要

这项研究旨在探究抗体调理的严重急性呼吸综合征冠状病毒2（SARS-CoV-2）与从人外周血单个核细胞（PBMC）中富集的单核细胞之间的相互作用，以确定抗体依赖增强作用是否可能导致2019冠状病毒病（COVID-19）的病理生理过程。将SARS-CoV-2与住院COVID-19患者的血清进行预孵育，导致单核细胞中的病毒摄取和病毒复制显著增加。值得注意的是，与重症COVID-19患者血清预孵育的SARS-CoV-2可强烈增加单核细胞分泌白细胞介素-6（IL-6），而与轻症患者血清或接种疫苗后血清预孵育的SARS-CoV-2则无此作用。单克隆抗FcγRIIa抗体可部分抑制抗体依赖的病毒摄取，而IL-6分泌则完全被消除。FcγRIIa优先结合IgG2，与轻症COVID-19病例相比，重症COVID-19患者血清中的IgG2水平较低，而IgG1水平升高。这些数据表明，FcγRIIa介导的抗体调理的SARS-CoV-2结合对单核细胞炎性细胞因子释放和COVID-19病理生理过程具有关键影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/18321a5d6446/eujmi-14-380-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/bc140fbc5dc6/eujmi-14-380-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/397130e76da2/eujmi-14-380-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/bc140fbc5dc6/eujmi-14-380-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/a2fa2b468624/eujmi-14-380-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5849/11836651/397130e76da2/eujmi-14-380-g003.jpg
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