Rapid isolation and immune profiling of SARS-CoV-2 specific memory B cell in convalescent COVID-19 patients via LIBRA-seq

文献类型： 外文期刊

第一作者： He, Bing

作者： He, Bing;Liu, Shuning;Wang, Yuanyuan;Xu, Mengxin;Cai, Wei;Bai, Wendi;Ma, Yong;Meng, Huicui;Li, Yanling;Luo, Huanle;Du, Xiangjun;Chen, Yao-Qing;Liu, Jia;Hu, Hengrui;Yang, Jingyi;Yan, Huimin;Wang, Manli;Ye, Shupei;Sun, Tao;Sun, Tao;Shi, Mang;Guo, Deyin;Zhao, Wenjing;Chen, Shoudeng;Zhu, Haipeng;Jie, Yusheng;Yang, Yuedong;Wang, Qiao;Liu, Yuwen;Liu, Yuwen;Liu, Yuwen;Chen, Yao-Qing

作者机构：

期刊名称：SIGNAL TRANSDUCTION AND TARGETED THERAPY （ 影响因子：18.187； 五年影响因子：21.177 ）

ISSN： 2095-9907

年卷期： 2021 年 6 卷 1 期

页码：

收录情况： SCI

摘要： B cell response plays a critical role against SARS-CoV-2 infection. However, little is known about the diversity and frequency of the paired SARS-CoV-2 antigen-specific BCR repertoire after SARS-CoV-2 infection. Here, we performed single-cell RNA sequencing and VDJ sequencing using the memory and plasma B cells isolated from five convalescent COVID-19 patients, and analyzed the spectrum and transcriptional heterogeneity of antibody immune responses. Via linking BCR to antigen specificity through sequencing (LIBRA-seq), we identified a distinct activated memory B cell subgroup (CD11c(high)CD95(high)) had a higher proportion of SARS-CoV-2 antigen-labeled cells compared with memory B cells. Our results revealed the diversity of paired BCR repertoire and the non-stochastic pairing of SARS-CoV-2 antigen-specific immunoglobulin heavy and light chains after SARS-CoV-2 infection. The public antibody clonotypes were shared by distinct convalescent individuals. Moreover, several antibodies isolated by LIBRA-seq showed high binding affinity against SARS-CoV-2 receptor-binding domain (RBD) or nucleoprotein (NP) via ELISA assay. Two RBD-reactive antibodies C14646P3S and C2767P3S isolated by LIBRA-seq exhibited high neutralizing activities against both pseudotyped and authentic SARS-CoV-2 viruses in vitro. Our study provides fundamental insights into B cell response following SARS-CoV-2 infection at the single-cell level.

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