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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
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 rec...
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Published in: | Virology (New York, N.Y.) N.Y.), 2017-12, Vol.512, p.1-7 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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.
•CCR1 and CCR2 expression is up-regulated in ex vivo PB B cells upon EBV infection.•CCR1 and CCR2B ORF transcripts were detected in lymphoblastoid cell lines (LCLs).•CCR1 and CCR2 proteins are up-regulated and functional in established LCLs.•CCR1 and CCR2A/B ORF transcripts were not detected in Burkitt lymphoma cell lines.•CCR1/CCR2B can be involved in the clearing EBV-infected latency III B cells. |
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ISSN: | 0042-6822 1096-0341 1096-0341 |
DOI: | 10.1016/j.virol.2017.08.034 |