TY - JOUR
T1 - Inhibition of macrophage inflammatory protein-1α production by Epstein-Barr virus
AU - Jabs, Wolfram J.
AU - Wagner, Hans J.
AU - Maurmann, Susanne
AU - Hennig, Holger
AU - Kreft, Burkhard
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2002/3/1
Y1 - 2002/3/1
N2 - Infection with Epstein-Barr virus (EBV) exerts substantially immunomodulating activities in vitro and in vivo. In this context, EBV-induced chemokine production and the influence of EBV on this highly redundant system of inflammatory proteins have hardly been investigated. This study analyzed the production of interleukin-8, RANTES, monocyte chemotactic protein-1, and macrophage inflammatory protein-1α (MIP-1α) on EBV infection of peripheral blood mononuclear cells from immune EBV-seropositive (EBV+) and noninfected EBV-seronegative (EBV-) individuals. EBV failed to induce the production of MIP-1α in EBV+ as well as EBV- individuals, whereas the other chemokines studied were readily expressed. Moreover, EBV completely down-regulated lipopolysaccharide (LPS)- and phytohemagglutinin-induced MIP-1α production up to 4 hours after induction. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of EBV- and LPS-stimulated cultures revealed that EBV inhibited MIP-1α production on the transcriptional level. This effect was abolished by addition of antiglycoprotein (gp)350/220, a monoclonal antibody against EBV's major envelope glycoprotein, which mediates binding of the virus to the EBV receptor, CD21. However, recombinant gp350/220 protein alone did not inhibit the LPS-induced MIP-1α production, indicating that infection of the target cell is indispensable for this effect. In summary, we demonstrate a new immunomodulating activity of EBV on the chemokine system that probably helps the virus to evade the host's immune system favoring lifelong infection.
AB - Infection with Epstein-Barr virus (EBV) exerts substantially immunomodulating activities in vitro and in vivo. In this context, EBV-induced chemokine production and the influence of EBV on this highly redundant system of inflammatory proteins have hardly been investigated. This study analyzed the production of interleukin-8, RANTES, monocyte chemotactic protein-1, and macrophage inflammatory protein-1α (MIP-1α) on EBV infection of peripheral blood mononuclear cells from immune EBV-seropositive (EBV+) and noninfected EBV-seronegative (EBV-) individuals. EBV failed to induce the production of MIP-1α in EBV+ as well as EBV- individuals, whereas the other chemokines studied were readily expressed. Moreover, EBV completely down-regulated lipopolysaccharide (LPS)- and phytohemagglutinin-induced MIP-1α production up to 4 hours after induction. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of EBV- and LPS-stimulated cultures revealed that EBV inhibited MIP-1α production on the transcriptional level. This effect was abolished by addition of antiglycoprotein (gp)350/220, a monoclonal antibody against EBV's major envelope glycoprotein, which mediates binding of the virus to the EBV receptor, CD21. However, recombinant gp350/220 protein alone did not inhibit the LPS-induced MIP-1α production, indicating that infection of the target cell is indispensable for this effect. In summary, we demonstrate a new immunomodulating activity of EBV on the chemokine system that probably helps the virus to evade the host's immune system favoring lifelong infection.
UR - http://www.scopus.com/inward/record.url?scp=0036493570&partnerID=8YFLogxK
U2 - 10.1182/blood.V99.5.1512
DO - 10.1182/blood.V99.5.1512
M3 - Journal articles
C2 - 11861262
AN - SCOPUS:0036493570
SN - 0006-4971
VL - 99
SP - 1512
EP - 1516
JO - Blood
JF - Blood
IS - 5
ER -
