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http://purl.uniprot.org/citations/27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27311858http://www.w3.org/2000/01/rdf-schema#comment"Interleukin-17A (IL-17A) is known to induce inflammatory responses and to be involved in the pathogenesis of not only autoimmune diseases, but also several metabolic and infectious diseases. In this study, IL-17A is shown to induce IL-6 expression in 3T3-L1 mature adipocytes. Interestingly, we found that IL-17A synergistically amplified TNFα-induced secretion of IL-6 and upregulation of IL-17RA expression in 3T3-L1 adipocytes. Its synergistic effects on IL-6 production were inhibited by pre-treatment with inhibitors of IκBα and JNK. Furthermore, IL-17A cooperatively enhanced LPS-mediated IL-6 production in 3T3-L1 adipocytes co-cultured with RAW264.7 macrophages. In addition, IL-17A also enhanced CCL20 production in 3T3-L1 adipocytes stimulated with TNFα or co-cultured with LPS-stimulated RAW macrophages. In high-fat diet-fed mouse epididymal adipose tissues, IL-17RA and RORγt mRNA levels were significantly increased and the serum level of CCL20 was also upregulated. Taken together, these data show that, in adipose tissues, IL-17A contributes to exacerbating insulin resistance-enhancing IL-6 production and promotes the infiltration of Th17 cells in cooperation with TNFα; these findings represent a novel hypothesis for the association between IL-17A-producing cells and type 2 diabetes."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2016.06.049"xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Yamashita A."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Sano T."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Asano T."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Iwashita M."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Sanui T."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Nishimura F."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Tsuruta M."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Matsunaga H."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/author"Shinjo T."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/name"Biochem Biophys Res Commun"xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/pages"241-246"xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/title"IL-17A synergistically enhances TNFalpha-induced IL-6 and CCL20 production in 3T3-L1 adipocytes."xsd:string
http://purl.uniprot.org/citations/27311858http://purl.uniprot.org/core/volume"477"xsd:string
http://purl.uniprot.org/citations/27311858http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/27311858
http://purl.uniprot.org/citations/27311858http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/27311858
http://purl.uniprot.org/uniprot/#_A0A0G2JGF4-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858
http://purl.uniprot.org/uniprot/#_Q0PMN1-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858
http://purl.uniprot.org/uniprot/#_Q0X0E6-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858
http://purl.uniprot.org/uniprot/#_A0A0G2JFG1-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858
http://purl.uniprot.org/uniprot/#_A0A0G2JFT1-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858
http://purl.uniprot.org/uniprot/#_A0A0R4J210-mappedCitation-27311858http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/27311858