Abstract
The newly identified cytokines, IL-28/IL-29 (also termed type III IFNs), are able to inhibit a number of viruses. Here, we examined the antiviral effects of IL-29/IL-28A against herpes simplex virus type 1 (HSV-1) in human NT2-N neurons and CHP212 neuronal cells. Both IL-29 and IL-28A could efficiently inhibit HSV-1 replication in neuronal cells, as evidenced by the reduced expression of HSV-1 DNA and proteins. This inhibitory effect of IL-29 and IL-28A against HSV-1 could be partially blocked by antibody to IL-10Rβ, one of the key receptors for IL-29 and IL-28A. To explore the underlying antiviral mechanisms employed by IL-29/IL-28A, we showed that IL-29/IL-28A could selectively induce the expression of several Toll-like receptors (TLRs) as well as activate TLR-mediated antiviral pathway, including IFN regulatory factor 7, IFN-α, and the key IFN-α stimulated antiviral genes.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies, Neutralizing / immunology
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Antibodies, Neutralizing / pharmacology
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Cell Line, Tumor
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DNA, Viral / biosynthesis
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Herpes Simplex / immunology*
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Herpes Simplex / pathology
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Herpes Simplex / virology
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Herpesvirus 1, Human / physiology*
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Humans
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Immunohistochemistry
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Interferon Regulatory Factor-7 / biosynthesis
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Interferon-alpha / biosynthesis
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Interferons
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Interleukins / biosynthesis
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Interleukins / immunology*
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Neurons / immunology*
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Neurons / pathology
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Neurons / virology
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Receptors, Interleukin-10 / antagonists & inhibitors*
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Receptors, Interleukin-10 / immunology
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Toll-Like Receptors / immunology
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Toll-Like Receptors / metabolism
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Up-Regulation
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Virus Replication / drug effects
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Virus Replication / immunology
Substances
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Antibodies, Neutralizing
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DNA, Viral
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interferon-lambda, human
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Interferon Regulatory Factor-7
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Interferon-alpha
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Interleukins
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Receptors, Interleukin-10
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Toll-Like Receptors
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Interferons