http://purl.uniprot.org/citations/23960239 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23960239 | http://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/23960239 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1300419"xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Singh S.P."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Steinman L."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Mountz J.D."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Steele C."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Raman C."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Cashman K.S."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "De Sarno P."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Naves R."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Axtell R.C."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/author | "Rowse A.L."xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
http://purl.uniprot.org/citations/23960239 | http://purl.uniprot.org/core/pages | "2967-2977"xsd:string |
http://purl.uniprot.org/citations/23960239 | http://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/23960239 | http://purl.uniprot.org/core/volume | "191"xsd:string |
http://purl.uniprot.org/citations/23960239 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23960239 |
http://purl.uniprot.org/citations/23960239 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23960239 |
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