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http://purl.uniprot.org/citations/25412660http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25412660http://www.w3.org/2000/01/rdf-schema#comment"T helper (TH)-cell subsets, such as TH1 and TH17, mediate inflammation in both peripheral tissues and central nervous system. Here we show that STAT5 is required for T helper-cell pathogenicity in autoimmune neuroinflammation but not in experimental colitis. Although STAT5 promotes regulatory T cell generation and immune suppression, loss of STAT5 in CD4+ T cells resulted in diminished development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Our results showed that loss of encephalitogenic activity of STAT5-deficient autoreactive CD4+ T cells was independent of IFN-γ or interleukin 17 (IL-17) production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), a crucial mediator of T-cell pathogenicity. We further showed that IL-7-activated STAT5 promotes the generation of GM-CSF-producing CD4+ T cells, which were preferentially able to induce more severe EAE than TH17 or TH1 cells. Consistent with GM-CSF-producing cells being a distinct subset of TH cells, the differentiation program of these cells was distinct from that of TH17 or TH1 cells. We further found that IL-3 was secreted in a similar pattern as GM-CSF in this subset of TH cells. In conclusion, the IL-7-STAT5 axis promotes the generation of GM-CSF/IL-3-producing TH cells. These cells display a distinct transcriptional profile and may represent a novel subset of T helper cells which we designate as TH-GM."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.org/dc/terms/identifier"doi:10.1038/cr.2014.154"xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Tan P."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Yang H."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Yang F."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Zhou Y."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Kaplan M.H."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Sheng W."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Kemeny D.M."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Fu X.Y."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Moh A."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/author"Low P.Y."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/name"Cell Res"xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/pages"1387-1402"xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/title"STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation."xsd:string
http://purl.uniprot.org/citations/25412660http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/25412660http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25412660
http://purl.uniprot.org/citations/25412660http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25412660
http://purl.uniprot.org/uniprot/#_B2C3G8-mappedCitation-25412660http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25412660
http://purl.uniprot.org/uniprot/#_Q14AD9-mappedCitation-25412660http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25412660
http://purl.uniprot.org/uniprot/#_Q71UV3-mappedCitation-25412660http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25412660
http://purl.uniprot.org/uniprot/#_Q3UZ79-mappedCitation-25412660http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25412660