Next Article in Journal
Complete Nucleotide Sequence Analysis of a Novel Bacillus subtilis-Infecting Bacteriophage BSP10 and Its Effect on Poly-Gamma-Glutamic Acid Degradation
Previous Article in Journal
Phytohormone Signaling of the Resistance to Plum pox virus (PPV, Sharka Disease) Induced by Almond (Prunus dulcis (Miller) Webb) Grafting to Peach (P. persica L. Batsch)
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessBrief Report
Viruses 2018, 10(5), 239; https://doi.org/10.3390/v10050239

Upregulation of the Chemokine Receptor CCR2B in Epstein‒Barr Virus-Positive Burkitt Lymphoma Cell Lines with the Latency III Program

1
August Kirchenstein Institute of Microbiology and Virology, Riga Stradins University, 5 Ratsupites Str, 1067 Riga, Latvia
2
Latvian Biomedical Research and Study Centre, 1 Ratsupites Str k-1, 1067 Riga, Latvia
3
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, 16 Nobelsväg, Box 280, 171 77 Stockholm, Sweden
4
R.E. Kavetsky Institute of Experimental Pathology, Oncology, and Radiobiology, NASU, 45 Vasylkivska str, 03022 Kyiv, Ukraine
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 9 April 2018 / Revised: 28 April 2018 / Accepted: 29 April 2018 / Published: 3 May 2018
(This article belongs to the Section Animal Viruses)
Full-Text   |   PDF [2810 KB, uploaded 7 May 2018]   |  

Abstract

CCR2 is the cognate receptor to the chemokine CCL2. CCR2–CCL2 signaling mediates cancer progression and metastasis dissemination. However, the role of CCR2–CCL2 signaling in pathogenesis of B-cell malignancies is not clear. Previously, we showed that CCR2B was upregulated in ex vivo peripheral blood B cells upon Epstein‒Barr virus (EBV) infection and in established lymphoblastoid cell lines with the EBV latency III program. EBV latency III is associated with B-cell lymphomas in immunosuppressed patients. The majority of EBV-positive Burkitt lymphoma (BL) tumors are characterized by latency I, but the BL cell lines drift towards latency III during in vitro culture. In this study, the CCR2A and CCR2B expression was assessed in the isogenic EBV-positive BL cell lines with latency I and III using RT-PCR, immunoblotting, and immunostaining analyses. We found that CCR2B is upregulated in the EBV-positive BL cells with latency III. Consequently, we detected the migration of latency III cells toward CCL2. Notably, the G190A mutation, corresponding to SNP CCR2-V64I, was found in one latency III cell line with a reduced migratory response to CCL2. The upregulation of CCR2B may contribute to the enhanced migration of malignant B cells into CCL2-rich compartments. View Full-Text
Keywords: CCR2; EBV; latency III; Burkitt lymphoma cell lines; B-cell lymphoma CCR2; EBV; latency III; Burkitt lymphoma cell lines; B-cell lymphoma
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Kozireva, S.; Rudevica, Z.; Baryshev, M.; Leonciks, A.; Kashuba, E.; Kholodnyuk, I. Upregulation of the Chemokine Receptor CCR2B in Epstein‒Barr Virus-Positive Burkitt Lymphoma Cell Lines with the Latency III Program. Viruses 2018, 10, 239.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Viruses EISSN 1999-4915 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top