Epstein-Barr virus encoded interleukin-10 inhibits HLA-class I, ICAM-1, and B7 expression on human monocytes: implications for immune evasion by EBV.

2.50
Hdl Handle:
http://hdl.handle.net/10541/84336
Title:
Epstein-Barr virus encoded interleukin-10 inhibits HLA-class I, ICAM-1, and B7 expression on human monocytes: implications for immune evasion by EBV.
Authors:
Salek-Ardakani, Shahram; Arrand, John R; Mackett, Mike
Abstract:
Monocytes and macrophages play a central role in viral infections, as a target for viruses and in activation of both innate and adaptive immune responses. Epstein-Barr virus (EBV) has evolved elaborate strategies to dampen the immune system and to persist within the host. There is evidence that the product of the BCRF-1 open reading frame of EBV, viral interleukin-10 (vIL-10), inhibits the capacity of monocytes/macrophages to induce T cell activation, but the full mechanism of this effect is unknown. To determine whether this effect might involve modulation of the expression of accessory molecules known to be important in T cell activation, we analyzed by flow cytometry the influence of vIL-10 on the basal as well as on IFN-gamma-induced up-regulation of HLA molecules, ICAM-1, and two members of the B7 family B7.1 (CD80) and B7.2 (CD86) at the surface of human monocytes. Viral IL-10 in a concentration-dependent manner inhibited both basal- and IFN-gamma-induced HLA-class II, ICAM-1 (basal levels of ICAM-2 and ICAM-3 is unaffected), CD80, and CD86 up-regulation when added simultaneously with IFN-gamma. In contrast, complete inhibition of HLA-class I expression on monocytes/macrophages occurred only when vIL-10 was present 2 h prior to the addition of IFN-gamma, implying that vIL-10 affects an early step in the IFN-gamma signaling pathway. As both monocytes and macrophages can be infected by EBV, we propose that vIL-10-mediated impairment of monocyte/macrophage antigen-presenting function could help the virus-infected cells to avoid detection by the host's T cells on one hand and contribute to its immunosuppressive properties on the other.
Affiliation:
Department of Molecular Biology, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester, M20 9BX United Kingdom. ssalek@liai.org
Citation:
Epstein-Barr virus encoded interleukin-10 inhibits HLA-class I, ICAM-1, and B7 expression on human monocytes: implications for immune evasion by EBV. 2002, 304 (2):342-51 Virology
Journal:
Virology
Issue Date:
20-Dec-2002
URI:
http://hdl.handle.net/10541/84336
DOI:
10.1006/viro.2002.1716
PubMed ID:
12504574
Type:
Article
Language:
en
ISSN:
0042-6822
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorSalek-Ardakani, Shahramen
dc.contributor.authorArrand, John Ren
dc.contributor.authorMackett, Mikeen
dc.date.accessioned2009-10-16T11:09:33Z-
dc.date.available2009-10-16T11:09:33Z-
dc.date.issued2002-12-20-
dc.identifier.citationEpstein-Barr virus encoded interleukin-10 inhibits HLA-class I, ICAM-1, and B7 expression on human monocytes: implications for immune evasion by EBV. 2002, 304 (2):342-51 Virologyen
dc.identifier.issn0042-6822-
dc.identifier.pmid12504574-
dc.identifier.doi10.1006/viro.2002.1716-
dc.identifier.urihttp://hdl.handle.net/10541/84336-
dc.description.abstractMonocytes and macrophages play a central role in viral infections, as a target for viruses and in activation of both innate and adaptive immune responses. Epstein-Barr virus (EBV) has evolved elaborate strategies to dampen the immune system and to persist within the host. There is evidence that the product of the BCRF-1 open reading frame of EBV, viral interleukin-10 (vIL-10), inhibits the capacity of monocytes/macrophages to induce T cell activation, but the full mechanism of this effect is unknown. To determine whether this effect might involve modulation of the expression of accessory molecules known to be important in T cell activation, we analyzed by flow cytometry the influence of vIL-10 on the basal as well as on IFN-gamma-induced up-regulation of HLA molecules, ICAM-1, and two members of the B7 family B7.1 (CD80) and B7.2 (CD86) at the surface of human monocytes. Viral IL-10 in a concentration-dependent manner inhibited both basal- and IFN-gamma-induced HLA-class II, ICAM-1 (basal levels of ICAM-2 and ICAM-3 is unaffected), CD80, and CD86 up-regulation when added simultaneously with IFN-gamma. In contrast, complete inhibition of HLA-class I expression on monocytes/macrophages occurred only when vIL-10 was present 2 h prior to the addition of IFN-gamma, implying that vIL-10 affects an early step in the IFN-gamma signaling pathway. As both monocytes and macrophages can be infected by EBV, we propose that vIL-10-mediated impairment of monocyte/macrophage antigen-presenting function could help the virus-infected cells to avoid detection by the host's T cells on one hand and contribute to its immunosuppressive properties on the other.en
dc.language.isoenen
dc.subject.meshAntigen Presentation-
dc.subject.meshAntigens, CD-
dc.subject.meshAntigens, CD80-
dc.subject.meshAntigens, CD86-
dc.subject.meshCells, Cultured-
dc.subject.meshHerpesvirus 4, Human-
dc.subject.meshHistocompatibility Antigens Class I-
dc.subject.meshHistocompatibility Antigens Class II-
dc.subject.meshHumans-
dc.subject.meshIntercellular Adhesion Molecule-1-
dc.subject.meshInterferon-gamma-
dc.subject.meshInterleukin-10-
dc.subject.meshMacrophages-
dc.subject.meshMembrane Glycoproteins-
dc.subject.meshMonocytes-
dc.subject.meshViral Proteins-
dc.titleEpstein-Barr virus encoded interleukin-10 inhibits HLA-class I, ICAM-1, and B7 expression on human monocytes: implications for immune evasion by EBV.en
dc.typeArticleen
dc.contributor.departmentDepartment of Molecular Biology, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester, M20 9BX United Kingdom. ssalek@liai.orgen
dc.identifier.journalVirologyen

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