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http://purl.uniprot.org/citations/14568135http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14568135http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14568135http://www.w3.org/2000/01/rdf-schema#comment"IL-23 and IL-12 are functionally related heterodimeric cytokines that share the IL-12p40 subunit. IL-23 and IL-12 function through heterodimeric receptors, which share the IL-12Rbeta1 subunit. Production of IL-23, a heterodimer of IL-12p40 and IL-23p19, by CNS antigen-presenting cells (APC) is critical for susceptibility to experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis (MS). We report that the expression of IL-23p19 mRNA is highly induced by stimulation with IFN-gamma and LPS in adult mouse microglia and a microglia cell line, EOC13. Expression of the IL-12R subunits, IL-12Rbeta1 and IL-12Rbeta2, is upregulated in both microglia and splenic macrophages upon stimulation with LPS or IFN-gamma and LPS, whereas the IL-23R subunit is upregulated only in macrophages. In EAE, an early peak of IL-23p19 mRNA expression is found in CD11b(+) CNS APC, compared with peripheral macrophages. In contrast, IL-12p40 and IL-12p35 mRNA maximum levels in the CNS are detected at peak of disease. The expression of IL-12p35 mRNA is more sustained than that of IL-12p40 and IL-23p19. Thus, IL-23 produced by CNS microglia/macrophages may contribute to the early induction of EAE. In the CNS, IL-23 may preferentially target infiltrating mononuclear cells, which upregulate IL-23R, rather than parenchymal microglia."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.org/dc/terms/identifier"doi:10.1016/s0022-510x(03)00203-x"xsd:string
http://purl.uniprot.org/citations/14568135http://purl.org/dc/terms/identifier"doi:10.1016/s0022-510x(03)00203-x"xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Gran B."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Gran B."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Kamoun M."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Kamoun M."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Rostami A."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Rostami A."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Siglienti I."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Siglienti I."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Ventura E.S."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Ventura E.S."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Zhang G.-X."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/author"Zhang G.-X."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/name"J. Neurol. Sci."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/name"J. Neurol. Sci."xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/pages"95-103"xsd:string
http://purl.uniprot.org/citations/14568135http://purl.uniprot.org/core/pages"95-103"xsd:string