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http://purl.uniprot.org/citations/29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29562202http://www.w3.org/2000/01/rdf-schema#comment"The death receptor Fas removes activated lymphocytes through apoptosis. Previous transcriptional profiling predicted that Fas positively regulates interleukin-17 (IL-17)-producing T helper 17 (Th17) cells. Here, we demonstrate that Fas promoted the generation and stability of Th17 cells and prevented their differentiation into Th1 cells. Mice with T-cell- and Th17-cell-specific deletion of Fas were protected from induced autoimmunity, and Th17 cell differentiation and stability were impaired. Fas-deficient Th17 cells instead developed a Th1-cell-like transcriptional profile, which a new algorithm predicted to depend on STAT1. Experimentally, Fas indeed bound and sequestered STAT1, and Fas deficiency enhanced IL-6-induced STAT1 activation and nuclear translocation, whereas deficiency of STAT1 reversed the transcriptional changes induced by Fas deficiency. Thus, our computational and experimental approach identified Fas as a regulator of the Th17-to-Th1 cell balance by controlling the availability of opposing STAT1 and STAT3 to have a direct impact on autoimmunity."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2018.03.008"xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Lee Y."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Regev A."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Wang C."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Przybylski D."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Kuchroo V.K."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Meyer Zu Horste G."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Sobel R."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Schnell A."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/author"Schramm M.A."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/pages"556-569.e7"xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/title"Fas Promotes T Helper 17 Cell Differentiation and Inhibits T Helper 1 Cell Development by Binding and Sequestering Transcription Factor STAT1."xsd:string
http://purl.uniprot.org/citations/29562202http://purl.uniprot.org/core/volume"48"xsd:string
http://purl.uniprot.org/citations/29562202http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29562202
http://purl.uniprot.org/citations/29562202http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29562202
http://purl.uniprot.org/uniprot/#_A0A087WSP5-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202
http://purl.uniprot.org/uniprot/#_A0A1L1ST40-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202
http://purl.uniprot.org/uniprot/#_A0A1L1SUX8-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202
http://purl.uniprot.org/uniprot/#_A0A087WRI1-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202
http://purl.uniprot.org/uniprot/#_A0A087WSQ5-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202
http://purl.uniprot.org/uniprot/#_P70677-mappedCitation-29562202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29562202