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http://purl.uniprot.org/citations/22184727http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22184727http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22184727http://www.w3.org/2000/01/rdf-schema#comment"Altered T cell function in systemic lupus erythematosus (SLE) is determined by various molecular and cellular abnormalities, including increased IL-17 production. Recent evidence suggests a crucial role for signaling lymphocyte activation molecules (SLAMs) in the expression of autoimmunity. In this study, we demonstrate that SLAMF3 and SLAMF6 expression is increased on the surface of SLE T cells compared with normal cells. SLAM coengagement with CD3 under Th17 polarizing conditions results in increased IL-17 production. SLAMF3 and SLAMF6 T cell surface expression and IL-17 levels significantly correlate with disease activity in SLE patients. Both naive and memory CD4(+) T cells produce more IL-17 in response to SLAM costimulation as compared with CD28 costimulation. In naive CD4(+) cells, IL-17 production after CD28 costimulation peaks on day 3, whereas costimulation with anti-SLAMF3 and anti-SLAMF6 Abs results in a prolonged and yet increasing production during 6 d. Unlike costimulation with anti-CD28, SLAM costimulation requires the presence of the adaptor molecule SLAM-associated protein. Thus, engagement of SLAMF3 and SLAMF6 along with Ag-mediated CD3/TCR stimulation represents an important source of IL-17 production, and disruption of this interaction with decoy receptors or blocking Abs should mitigate disease expression in SLE and other autoimmune conditions."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1102773"xsd:string
http://purl.uniprot.org/citations/22184727http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.1102773"xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Tsokos G.C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Tsokos G.C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Chatterjee M."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Chatterjee M."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Terhorst C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Terhorst C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Hedrich C.M."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Hedrich C.M."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Kis-Toth K."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Kis-Toth K."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Kyttaris V.C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Kyttaris V.C."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Rauen T."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/author"Rauen T."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/pages"1206-1212"xsd:string
http://purl.uniprot.org/citations/22184727http://purl.uniprot.org/core/pages"1206-1212"xsd:string