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在EB病毒感染时,外周血B细胞以及已建立的淋巴母细胞系中趋化因子受体CCR1和CCR2B的表达上调。

Expression of the chemokine receptors CCR1 and CCR2B is up-regulated in peripheral blood B cells upon EBV infection and in established lymphoblastoid cell lines.

作者信息

Kholodnyuk Irina, Rudevica Zanna, Leonciks Ainars, Ehlin-Henriksson Barbro, Kashuba Elena

机构信息

A. Kirchenstein Institute of Microbiology and Virology, Riga Stradins University (RSU), 5 Ratsupites str, 1067 Riga, Latvia; Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, 16 Nobels väg, Box 280, 171 77 Stockholm, Sweden.

Latvian Biomedical Research and Study Center, 1-1k Ratsupites str, 1067 Riga, Latvia.

出版信息

Virology. 2017 Dec;512:1-7. doi: 10.1016/j.virol.2017.08.034. Epub 2017 Sep 9.

Abstract

In immunocompetent individuals, EBV establishes in B cells an asymptomatic lifelong latent infection controlled by the immune system. Chemokine receptors regulate immune system function. CCR1 and CCR2 share protein sequence similarity and exert responses to multiple chemokines. The role of these receptors in B cells is largely unknown. We show that the mRNA and functional protein expression of CCR1 and CCR2 is induced in ex vivo B cells upon EBV infection and in established lymphoblastoid cell lines (LCLs). The CCR1 and CCR2B ORF transcripts were determined in LCLs. In contrast, in both the EBV-negative and EBV-positive Burkitt lymphoma cell lines, neither the CCR1, CCR2A, and CCR2B ORF transcripts nor their corresponding proteins were detected. Our data suggest that CCR1/CCR2B could be involved in clearing EBV-infected latency III B cells in immunocompetent individuals via directing the migration of these cells and attracting the chemokines-expressing immune cells.

摘要

在免疫功能正常的个体中,EB病毒在B细胞中建立一种由免疫系统控制的无症状终身潜伏感染。趋化因子受体调节免疫系统功能。CCR1和CCR2具有蛋白质序列相似性,并对多种趋化因子产生反应。这些受体在B细胞中的作用在很大程度上尚不清楚。我们发现,CCR1和CCR2的mRNA及功能性蛋白表达在EB病毒感染后的体外B细胞以及已建立的淋巴母细胞系(LCLs)中被诱导。在LCLs中测定了CCR1和CCR2B的开放阅读框转录本。相比之下,在EB病毒阴性和阳性的伯基特淋巴瘤细胞系中,均未检测到CCR1、CCR2A和CCR2B的开放阅读框转录本及其相应蛋白。我们的数据表明,CCR1/CCR2B可能通过引导这些细胞的迁移并吸引表达趋化因子的免疫细胞,参与清除免疫功能正常个体中被EB病毒感染的潜伏期III B细胞。

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