RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/24699451http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24699451http://www.w3.org/2000/01/rdf-schema#comment"TH1 and TH17 cells mediate neuroinflammation in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Pathogenic TH cells in EAE must produce the pro-inflammatory cytokine granulocyte-macrophage colony stimulating factor (GM-CSF). TH cell pathogenicity in EAE is also regulated by cell-intrinsic production of the immunosuppressive cytokine interleukin 10 (IL-10). Here we demonstrate that mice deficient for the basic helix-loop-helix (bHLH) transcription factor Bhlhe40 (Bhlhe40(-/-)) are resistant to the induction of EAE. Bhlhe40 is required in vivo in a T cell-intrinsic manner, where it positively regulates the production of GM-CSF and negatively regulates the production of IL-10. In vitro, GM-CSF secretion is selectively abrogated in polarized Bhlhe40(-/-) TH1 and TH17 cells, and these cells show increased production of IL-10. Blockade of IL-10 receptor in Bhlhe40(-/-) mice renders them susceptible to EAE. These findings identify Bhlhe40 as a critical regulator of autoreactive T-cell pathogenicity."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.org/dc/terms/identifier"doi:10.1038/ncomms4551"xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Cook L.E."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Carrero J.A."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Egawa T."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Lin C.C."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Bradstreet T.R."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Edelson B.T."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Murphy T.L."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Russell J.H."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Sim J."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Taneja R."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Chou C."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/author"Schwarzkopf E.A."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/pages"3551"xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/title"Bhlhe40 controls cytokine production by T cells and is essential for pathogenicity in autoimmune neuroinflammation."xsd:string
http://purl.uniprot.org/citations/24699451http://purl.uniprot.org/core/volume"5"xsd:string
http://purl.uniprot.org/citations/24699451http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24699451
http://purl.uniprot.org/citations/24699451http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24699451
http://purl.uniprot.org/uniprot/#_B3VI66-mappedCitation-24699451http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24699451
http://purl.uniprot.org/uniprot/#_E9Q2C3-mappedCitation-24699451http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24699451
http://purl.uniprot.org/uniprot/#_Q14AD9-mappedCitation-24699451http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24699451