ArticleMolecular immunology2009
Recombinant murine cytomegalovirus vector activates human monocyte-derived dendritic cells in a NF-kappaB dependent pathway.
Article in Molecular immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Uncovering the Anticancer Potential of Murine Cytomegalovirus against Human Colon Cancer Cells.Molecular therapy oncolytics · 2020Article
- Presentation of Cryptic Peptides by MHC Class I Is Enhanced by Inflammatory Stimuli.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Probability weighted ensemble transfer learning for predicting interactions between HIV-1 and human proteins.PloS one · 2013Article
- A novel biclustering approach to association rule mining for predicting HIV-1-human protein interactions.PloS one · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To evaluate the potential use of recombinant murine cytomegalovirus (MCMV) as an antigen delivery vector, we examined the cytokine and CD80 and CD86 expression profiles of MCMV encoding either enhanced green fluorescent protein gene (MCMV-EGFP) or human immunodeficiency virus-1 glycoprotein gp120 gene (MCMV-gp120) infected monocyte-derived dendritic cells (Mo-DC) and investigated the role of nuclear factor kappa B (NF-kappaB) in Mo-DC activation. Results showed that MCMV triggered the induction of inflammatory cytokines and/or CD80 and CD86 up-regulation in Mo-DC. UV-inactivated MCMV exhibited a reduced production of inflammatory cytokines and a lowered expression of CD80 and CD86 compared with live MCMV infection. Treatment of cells with a NF-kappaB peptide inhibitor prior to MCMV infection reduced the induction of cytokines and CD80 and CD86 up-regulation. Overall, the results suggest that recombinant MCMV vectors activate human Mo-DC in a NF-kappaB dependent pathway. The abortive infection or de novo gene expression greatly enhances the activation of Mo-DC by MCMV vectors.
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Registered trials
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