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Campo DC | Valor | Lengua/Idioma |
---|---|---|
dc.creator | Larrea, E. (Esther) | - |
dc.creator | Aldabe, R. (Rafael) | - |
dc.creator | Gonzalez, I. (Iranzu) | - |
dc.creator | Segura, V. (Víctor) | - |
dc.creator | Sarobe, P. (Pablo) | - |
dc.creator | Echeverria, I. (Itziar) | - |
dc.creator | Prieto, J. (Jesús) | - |
dc.date.accessioned | 2012-04-04T12:16:32Z | - |
dc.date.available | 2012-04-04T12:16:32Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | Larrea E, Aldabe R, Gonzalez I, Segura V, Sarobe P, Echeverria I, et al. Oncostatin M enhances the antiviral effects of type I interferon and activates immunostimulatory functions in liver epithelial cells. J Virol 2009 Apr;83(7):3298-3311. | es_ES |
dc.identifier.issn | 1098-5514 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21601 | - |
dc.description.abstract | Oncostatin M (OSM) is released together with type I interferon (IFN) by activated dendritic cells, suggesting a concerted action of these cytokines in the biological response against infection. We found that OSM increases the antiviral effect of IFN-alpha in Huh7 hepatoma cells infected with hepatitis A or hepatitis C virus and synergizes with IFN-alpha in the induction of antiviral genes. The combination of OSM and IFN-alpha led to upregulation of both STAT1 and STAT3 together with intense and prolonged activation of STAT1, STAT3, and Jak1. OSM with or without IFN-alpha also activated p38 mitogen-activated protein kinase, which is known to enhance transcription of IFN-alpha-inducible genes. Interestingly, OSM combined with IFN-alpha strongly induced immunoproteasome genes and other genes involved in antigen processing and presentation. Moreover, OSM, alone or in combination with IFN-alpha, upregulated relevant innate immunity molecules and increased the expression of intracellular adhesion molecule 1 and interleukin-15 receptor alpha (IL-15Ralpha) in liver cells. Hepatoma cells transfected with a plasmid encoding a viral antigen were able to activate effector T cells when pretreated with IFN-alpha plus OSM but not with each cytokine separately. Also, OSM, more than IFN-alpha, augmented the ability of Huh7 cells to transpresent IL-15 to responding lymphocytes and increased the immunostimulatory activity of liver epithelial cells by presenting a short viral peptide to sensitized cytotoxic T cells. In conclusion, OSM enhances the antiviral effects of type I interferon and cooperates with it in the induction of adaptive immune responses to pathogens. These findings may have therapeutic implications. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Society for Microbiology | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Epithelial Cells/immunology | es_ES |
dc.subject | Hepacivirus/immunology | es_ES |
dc.subject | Hepatitis A virus/immunology | es_ES |
dc.subject | Interferon Type I/immunology | es_ES |
dc.subject | Liver/immunology | es_ES |
dc.subject | Oncostatin M/immunology | es_ES |
dc.title | Oncostatin M enhances the antiviral effects of type I interferon and activates immunostimulatory functions in liver epithelial cells | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://jvi.asm.org/content/83/7/3298 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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