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http://purl.uniprot.org/citations/26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26059829http://www.w3.org/2000/01/rdf-schema#comment"MS is an autoimmune disease characterized by immune cell infiltration in the CNS, leading to cumulative disability. IFN-β, used clinically in RR-MS reduces lesion formation and rates of relapse. Although the molecular mechanisms are not entirely elucidated, myeloid cells appear to be a major target for the therapeutic effects of IFN-β. DCs have a critical role in experimental models of MS through their effect on encephalitogenic Th1/Th17 cell differentiation and expansion. Here we focused on the effects of IFN-β on DC expression of cytokines involved in the control of Th1/Th17 differentiation and expansion. Administration of IFN-β to mice immunized with MOG35-55 inhibited IL-12 and IL-23 expression in splenic DC and reduced in vivo differentiation of Th1/Th17 cells. IFN-β affected cytokine expression in TLR-stimulated DC in a similar manner in vitro, inhibiting IL-12 and IL-23 and stimulating IL-10 at both mRNA and protein levels, by signaling through IFNAR. We investigated the role of the signaling molecules STAT1/STAT2, IRF-1 and IRF-7, and of the PI3K→GSK3 pathway. IFN-β inhibition of the IL-12 subunits p40 and p35 was mediated through STAT1/STAT2, whereas inhibition of IL-23 was STAT1 dependent, and the stimulatory effect on IL-10 expression was mediated through STAT2. IFN-β induces IRF-7 and, to a lesser degree, IRF-1. However, neither IRF mediated the effects of IFN-β on IL-12, IL-23, or IL-10. We found that the PI3K pathway mediated IL-12 inhibition but did not interfere with the inhibition of IL-23 or stimulation of IL-10."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.org/dc/terms/identifier"doi:10.1189/jlb.3hi0914-453r"xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Emig F."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Kong W."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Kuo P.C."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Ganea D."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Yen J.H."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Hooper K.M."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Rahbari K.M."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/author"Scofield B.A."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/name"J Leukoc Biol"xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/pages"689-702"xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/title"Differential effects of IFN-beta on IL-12, IL-23, and IL-10 expression in TLR-stimulated dendritic cells."xsd:string
http://purl.uniprot.org/citations/26059829http://purl.uniprot.org/core/volume"98"xsd:string
http://purl.uniprot.org/citations/26059829http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26059829
http://purl.uniprot.org/citations/26059829http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26059829
http://purl.uniprot.org/uniprot/#_A0A087WSP5-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_A0A087WRI1-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_A0A087WSQ5-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_P15314-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_A0A1B0GRH7-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_A0A7R8GUQ3-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829
http://purl.uniprot.org/uniprot/#_A0A338P6T9-mappedCitation-26059829http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26059829