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http://purl.uniprot.org/citations/18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18424756http://www.w3.org/2000/01/rdf-schema#comment"IL-27 is a member of the IL-12 family of cytokines that activates the Jak-STAT signaling pathway in a context-dependent manner and has pleiotropic effects on acquired immunity. IL-27 has the capacity to promote early stages of Th1 generation, but recent evidence has suggested a predominant suppressive effect on Th1, Th2, and Th17 differentiation. Although modest suppressive effects of IL-27 on myeloid lineage cells have been observed, there is limited knowledge about the role of IL-27 in the regulation of innate immunity. In this study we report that although in resting murine macrophages IL-27 had minimal if any effects, in resting human monocytes IL-27 had profound proinflammatory functions. IL-27 activated a STAT1-dominant pattern of signaling in human monocytes with the consequent activation of STAT1-dependent inflammatory target genes. IL-27 primed monocytes for augmented responses to TLR stimulation in a STAT1-dependent manner, altered IL-10 signaling, and attenuated IL-10-induced gene expression. Strikingly, IL-27 strongly suppressed TLR-induced IL-10 production in human monocytes. However, the proinflammatory effects of IL-27 on human monocytes were rapidly abrogated by LPS via a p38-mediated mechanism that inhibited IL-27 signaling. Our findings identify a predominantly proinflammatory function for IL-27 in human monocytes and suggest a mechanism by which the activating effects of IL-27 on innate immunity are attenuated as an immune response proceeds and IL-27 transitions to predominantly suppressive effects on acquired immunity."xsd:string
http://purl.uniprot.org/citations/18424756http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.180.9.6325"xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/author"Ivashkiv L.B."xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/author"Kalliolias G.D."xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/pages"6325-6333"xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/title"IL-27 activates human monocytes via STAT1 and suppresses IL-10 production but the inflammatory functions of IL-27 are abrogated by TLRs and p38."xsd:string
http://purl.uniprot.org/citations/18424756http://purl.uniprot.org/core/volume"180"xsd:string
http://purl.uniprot.org/citations/18424756http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18424756
http://purl.uniprot.org/citations/18424756http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18424756
http://purl.uniprot.org/uniprot/#_A0A510GDC6-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_A5D905-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_A0A510GDE6-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_B3VI66-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_D2KFR9-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_B4E0K5-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_B5TY33-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_P42224-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_Q15454-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_Q71UZ1-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_L7RSM2-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_Q16539-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756
http://purl.uniprot.org/uniprot/#_Q67C41-mappedCitation-18424756http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18424756