scholarly journals Expression of the Epstein-Barr Virus-Encoded Epstein-Barr Virus Nuclear Antigen 1 in Hodgkin's Lymphoma Cells Mediates Up-Regulation of CCL20 and the Migration of Regulatory T Cells

2008 ◽  
Vol 173 (1) ◽  
pp. 195-204 ◽  
Author(s):  
Karl R.N. Baumforth ◽  
Anna Birgersdotter ◽  
Gary M. Reynolds ◽  
Wenbin Wei ◽  
Georgia Kapatai ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Hodgkin’S Lymphoma ◽  
Epstein Barr Virus ◽  
Hodgkin's Lymphoma ◽  
Nuclear Antigen ◽  
Lymphoma Cells ◽  
Barr Virus ◽  
Epstein Barr

The relationships between Epstein-Barr virus latent membrane protein 1 and regulatory T cells in Hodgkin's lymphoma

2007 ◽  
Vol 35 (4) ◽  
pp. 596-604 ◽  
Author(s):  
Neil A. Marshall ◽  
Dominic J. Culligan ◽  
Jane Tighe ◽  
Peter W. Johnston ◽  
Robert N. Barker ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Hodgkin's Lymphoma ◽  
Latent Membrane Protein 1 ◽  
Barr Virus ◽  
Epstein Barr ◽  
Virus Latent Membrane Protein

Expression of Epstein-Barr virus replicative proteins in aids-related non-Hodgkin's lymphoma cells

1991 ◽  
Vol 165 (4) ◽  
pp. 289-299 ◽  
Author(s):  
Gorm Pallesen ◽  
Stephen J. Hamilton-Dutoit ◽  
Martin Rowe ◽  
Ida Lisse ◽  
Elisabeth Ralfkiaer ◽  
...  
Keyword(s):  
Hodgkin’S Lymphoma ◽  
Epstein Barr Virus ◽  
Hodgkin's Lymphoma ◽  
Lymphoma Cells ◽  
Barr Virus ◽  
Non Hodgkin’S Lymphoma ◽  
Non Hodgkin's Lymphoma ◽  
Epstein Barr

scholarly journals Comparison of three methods for the detection of Epstein-Barr virus in Hodgkin’s lymphoma in paraffin-embedded tissues

2012 ◽  
Vol 7 (1) ◽  
pp. 89-92 ◽  
Author(s):  
ZONG-LI QI ◽  
XI-QUN HAN ◽  
JUN HU ◽  
GUANG-HUA WANG ◽  
JIN-WEI GAO ◽  
...  
Keyword(s):  
Hodgkin’S Lymphoma ◽  
Epstein Barr Virus ◽  
Hodgkin's Lymphoma ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Association between Epstein-Barr virus and Hodgkin's lymphoma in Belgium: A pathological and virological study

2007 ◽  
Vol 48 (7) ◽  
pp. 1323-1331 ◽  
Author(s):  
Mounir Trimèche ◽  
Christophe Bonnet ◽  
Sadok Korbi ◽  
Jacques Boniver ◽  
Laurence de Leval
Keyword(s):  
Hodgkin’S Lymphoma ◽  
Epstein Barr Virus ◽  
Hodgkin's Lymphoma ◽  
Barr Virus ◽  
Virological Study ◽  
Epstein Barr

scholarly journals Selective Induction of Th2-Attracting Chemokines CCL17 and CCL22 in Human B Cells by Latent Membrane Protein 1 of Epstein-Barr Virus

2004 ◽  
Vol 78 (4) ◽  
pp. 1665-1674 ◽  
Author(s):  
Takashi Nakayama ◽  
Kunio Hieshima ◽  
Daisuke Nagakubo ◽  
Emiko Sato ◽  
Masahiro Nakayama ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Regulatory T Cells ◽  
Epstein Barr Virus ◽  
Cytotoxic T Cells ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr

ABSTRACT Chemokines are likely to play important roles in the pathophysiology of diseases associated with Epstein-Barr virus (EBV). Here, we have analyzed the repertoire of chemokines expressed by EBV-infected B cells. EBV infection of B cells induced expression of TARC/CCL17 and MDC/CCL22, which are known to attract Th2 cells and regulatory T cells via CCR4, and also upregulated constitutive expression of MIP-1α/CCL3, MIP-1β/CCL4, and RANTES/CCL5, which are known to attract Th1 cells and cytotoxic T cells via CCR5. Accordingly, EBV-immortalized B cells secreted these chemokines, especially CCL3, CCL4, and CCL22, in large quantities. EBV infection or stable expression of LMP1 also induced CCL17 and CCL22 in a B-cell line, BJAB. The inhibitors of the TRAF/NF-κB pathway (BAY11-7082) and the p38/ATF2 pathway (SB202190) selectively suppressed the expression of CCL17 and CCL22 in EBV-immortalized B cells and BJAB-LMP1. Consistently, transient-transfection assays using CCL22 promoter-reporter constructs demonstrated that two NF-κB sites and a single AP-1 site were involved in the activation of the CCL22 promoter by LMP1. Finally, serum CCL22 levels were significantly elevated in infectious mononucleosis. Collectively, LMP1 induces CCL17 and CCL22 in EBV-infected B cells via activation of NF-κB and probably ATF2. Production of CCL17 and CCL22, which attract Th2 and regulatory T cells, may help EBV-infected B cells evade immune surveillance by Th1 cells. However, the concomitant production of CCL3, CCL4, and CCL5 by EBV-infected B cells may eventually attract Th1 cells and cytotoxic T cells, leading to elimination of EBV-infected B cells at latency III and to selection of those with limited expression of latent genes.

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