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http://purl.uniprot.org/citations/23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23960239http://www.w3.org/2000/01/rdf-schema#comment"Type I IFNs (IFN-α and IFN-β) and type II IFN (IFN-γ) mediate both regulation and inflammation in multiple sclerosis, neuromyelitis optica, and in experimental autoimmune encephalomyelitis (EAE). However, the underlying mechanism for these Janus-like activities of type I and II IFNs in neuroinflammation remains unclear. Although endogenous type I IFN signaling provides a protective response in neuroinflammation, we find that when IFN-γ signaling is ablated, type I IFNs drive inflammation, resulting in exacerbated EAE. IFN-γ has a disease stage-specific opposing function in EAE. Treatment of mice with IFN-γ during the initiation phase of EAE leads to enhanced severity of disease. In contrast, IFN-γ treatment during the effector phase attenuated disease. This immunosuppressive activity of IFN-γ required functional type I IFN signaling. In IFN-α/β receptor-deficient mice, IFN-γ treatment during effector phase of EAE exacerbated disease. Using an adoptive transfer EAE model, we found that T cell-intrinsic type I and II IFN signals are simultaneously required to establish chronic EAE by encephalitogenic Th1 cells. However, in Th17 cells loss of either IFN signals leads to the development of a severe chronic disease. The data imply that type I and II IFN signals have independent but nonredundant roles in restraining encephalitogenic Th17 cells in vivo. Collectively, our data show that type I and II IFNs function in an integrated manner to regulate pathogenesis in EAE."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1300419"xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Singh S.P."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Steinman L."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Mountz J.D."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Steele C."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Raman C."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Cashman K.S."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"De Sarno P."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Naves R."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Axtell R.C."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/author"Rowse A.L."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/pages"2967-2977"xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/title"The interdependent, overlapping, and differential roles of type I and II IFNs in the pathogenesis of experimental autoimmune encephalomyelitis."xsd:string
http://purl.uniprot.org/citations/23960239http://purl.uniprot.org/core/volume"191"xsd:string
http://purl.uniprot.org/citations/23960239http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23960239
http://purl.uniprot.org/citations/23960239http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23960239
http://purl.uniprot.org/uniprot/#_P15261-mappedCitation-23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23960239
http://purl.uniprot.org/uniprot/#_A0A338P6T9-mappedCitation-23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23960239
http://purl.uniprot.org/uniprot/#_A0A338P6X7-mappedCitation-23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23960239
http://purl.uniprot.org/uniprot/#_A0A384DVB8-mappedCitation-23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23960239
http://purl.uniprot.org/uniprot/#_E9PWM1-mappedCitation-23960239http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23960239