Modulatory effects of human herpes virus-7 on cytokine synthesis and cell proliferation in human peripheral blood mononuclear cell cultures
Human herpes virus‐7 (HHV‐7) infects cells of the immune system and thus may modulate their function. To investigate the potential immunomodulatory effects of this virus, we performed an in vitro study in which we investigated effects of HHV‐7 on the synthesis of several key immunomodulatory cytokin...
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Published in | Journal of leukocyte biology Vol. 66; no. 5; pp. 822 - 828 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Society for Leukocyte Biology
01.11.1999
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Subjects | |
Online Access | Get full text |
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Summary: | Human herpes virus‐7 (HHV‐7) infects cells of the immune system and thus may modulate their function. To investigate the potential immunomodulatory effects of this virus, we performed an in vitro study in which we investigated effects of HHV‐7 on the synthesis of several key immunomodulatory cytokines, i.e. tumor necrosis factor α (TNF‐α), interleukin‐2 (IL‐2), interferon‐γ (IFN‐γ), IL‐4, IL‐6, and transforming growth factor β (TGF‐β). This was examined after in vitro infection of human peripheral blood mononuclear cells (PBMC) with HHV‐7. We found elevated levels of TNF‐α, TGF‐β, and IFN‐γ in the supernatants of HHV‐7‐infected cells. By reverse transcriptase‐polymerase chain reaction (RT‐PCR) analysis, using cytokine‐specific primers, we found that levels of TNF‐α, TGF‐β, and IFN‐γ mRNA were increased in the infected cells. The HHV‐7 infection also significantly (P < 0.05) decreased the production of IL‐2 from activated, IL‐2‐producing PBMC. Furthermore, mitogen‐ and cytokine‐induced cellular proliferative responses of human PBMC were found to be significantly (P < 0.05) down‐regulated by this virus. On the other hand, HHV‐7 did not affect IL‐4 and IL‐6 synthesis. Overall, our results indicate that HHV‐7 infection causes significant immunomodulatory effects with regard to cytokine synthesis in these cells as well as inhibiting lymphocyte proliferation by various stimuli. J. Leukoc. Biol. 66: 822–828; 1999. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0741-5400 1938-3673 |
DOI: | 10.1002/jlb.66.5.822 |