Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells

[img]
Preview
PDF (Original Article) - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
3MB
[img]
Preview
PDF (Supplementary Material) - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader
7MB

Item Type:Article
Title:LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells
Creators Name:Zhang, J. and Sommermann, T. and Li, X. and Gieselmann, L. and de la Rosa, K. and Stecklum, M. and Klein, F. and Kocks, C. and Rajewsky, K.
Abstract:INTRODUCTION: Epstein-Barr virus (EBV) infection in humans is associated with a wide range of diseases including malignancies of different origins, most prominently B cells. Several EBV latent genes are thought to act together in B cell immortalization, but a minimal set of EBV genes sufficient for transformation remains to be identified. METHODS: Here, we addressed this question by transducing human peripheral B cells from EBV-negative donors with retrovirus expressing the latent EBV genes encoding Latent Membrane Protein (LMP) 1 and 2A and Epstein-Barr Nuclear Antigen (EBNA) 2. RESULTS: LMP1 together with EBNA2, but not LMP1 alone or in combination with LMP2A was able to transform human primary B cells. LMP1/EBNA2-immortalized cell lines shared surface markers with EBV-transformed lymphoblastoid cell lines (LCLs). They showed sustained growth for more than 60 days, albeit at a lower growth rate than EBV-transformed LCLs. LMP1/EBNA2-immortalized cell lines generated tumors when transplanted subcutaneously into severely immunodeficient NOG mice. CONCLUSION: Our results identify a minimal set of EBV proteins sufficient for B cell transformation.
Keywords:B Cell Lymphoma, Lymphomagenesis, Epstein-Barr Virus (EBV), EBV Latent Genes, Epstein-Barr Nuclear Antigen 2 (EBNA2), Latent Membrane Protein 1 (LMP1), Lymphoblastoid Cell Line (LCL), Transduction of Human Primary B Cells, Animals, Mice
Source:Frontiers in Immunology
ISSN:1664-3224
Publisher:Frontiers Media SA
Volume:14
Page Range:1331730
Date:19 December 2023
Official Publication:https://doi.org/10.3389/fimmu.2023.1331730
PubMed:View item in PubMed

Repository Staff Only: item control page

Downloads

Downloads per month over past year

Open Access
MDC Library