| http://purl.uniprot.org/citations/21262564 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21262564 | http://www.w3.org/2000/01/rdf-schema#comment | "The absence of IFN-γ signaling leads to an increased inflammatory response in many murine models of autoimmune diseases induced by a CFA-assisted immunization schedule. We investigated the role of endogenous IFN-γ in arthritis induced by immunization with glucose-6-phosphate isomerase (G6PI) in CFA in DBA/1 mice. Surprisingly, and in contrast to our previous findings in collagen-induced arthritis (CIA), G6PI-induced arthritis was found to be reduced in IFN-γ receptor-deficient (IFN-γR KO) mice, demonstrating a proinflammatory role for IFN-γ in this model. Milder disease in IFN-γR KO mice was associated with less vigorous innate and adaptive immune responses early (day 9) after immunization: less proliferation of myeloid cells in the spleen, less osteoclast formation, less G6PI-reactive Th cells (as measured by ex vivo stimulation and flow cytometry and by in vivo skin reactivity to G6PI) and lower G6PI-specific immunoglobulin serum levels. Surprisingly, on day 21, despite continued milder disease in IFN-γR KO mice, their Th cell responses were no longer diminished but augmented as compared to wild-type mice, and their numbers of immature myeloid splenocytes were also more increased. These data reveal that IFN-γ signaling is critical for the induction of the early immune responses which trigger G6PI-induced arthritis. The strikingly different clinical consequences of absent IFN-γ signaling in G6PI-induced arthritis compared with the very similarly induced CIA emphasize that the role of a single cytokine in experimentally induced arthritis depends critically on the very nature of the inciting (auto)antigen and in particular on the kinetics of the disease manifestation elicited by the antigen."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.jaut.2010.12.006"xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Mitera T."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Kamradt T."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Matthys P."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Kelchtermans H."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Schurgers E."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/author | "Frey O."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/name | "J Autoimmun"xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/pages | "161-169"xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/title | "Ameliorated course of glucose-6-phosphate isomerase (G6PI)-induced arthritis in IFN-gamma receptor knockout mice exposes an arthritis-promoting role of IFN-gamma."xsd:string |
| http://purl.uniprot.org/citations/21262564 | http://purl.uniprot.org/core/volume | "36"xsd:string |
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