EBV Conference 2008 Guangzhou - Baylor College of Medicine

99 (RegID: 1135; 1136)
Liang Wu
Institution: Department of Microbiology, Tumour and Cell Biology, Karolinska Institutet
e-mail: wul2004@hotmail.com
POSSIBLE ROLE FOR EBERS IN THE REGULATION OF CCR7 EXPRESSION IN
EBV-INFECTED B CELLS
Wu Liang, George Klein, Anna Nilsson, Barbro Ehlin-Henriksson
Wu Liang1, George Klein1, Anna Nilsson1,2, Barbro Ehlin-Henriksson1
1Department of Microbiology, Tumour and Cell Biology, Karolinska Institutet, 171 77 Stockholm,
Sweden
2Pediatric Cancer Research Unit, Astrid Lindgrens Children Hospital, 171 76 Stockholm, Sweden
Posterabstract:
The Epstein-Barr virus-encoded proteins EBNA-2 and LMP1 have been shown to modulate the
expression of chemokine receptors CXCR4 and CCR7. These chemokine receptors play an essential role
in B cell trafficking and micro-anatomic organization of lymphoid tissues. Previously, it was shown that
introduction of EBNA-2 into the EBV-negative Burkitt lymphoma (BL) line BL41 resulted in the
up-regulation of CCR7. In the ER/EB2-5 system, where the EBNA-2 expression and activity is estrogen
dependent, CCR7 was down-regulated after 3 days of estrogen starvation. These data indicate that
EBNA-2 may play a role in the regulation of CCR7 expression.
We have investigated the CCR7 expression in tonsillar B cells after EBV infection. One week after
infection CCR7 expression was markedly decreased even though EBNA-2 was expressed. This
paradoxical result may be due to the involvement of other EBV-encoded proteins or miRNAs in the
primary infected B cells.
In the present study we have examined the effect of the EBV-encoded small RNAs, EBERs, on the
expression of CCR7 in the EBV-negative Akata BL transfected with an EBERs expression vector. CCR7
expression decreased in the EBERs-expressing BL cells in comparison with its control. This finding is
consistent with the possibility that EBERs may counteract the EBNA-2-mediated CCR7 induction in the
primary EBV-infected tonsillar B cells.
EBV Conference 2008 Guangzhou
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