RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/31139177http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31139177http://www.w3.org/2000/01/rdf-schema#comment"Thymic stromal lymphopoietin (TSLP) is a functionally pleotropic cytokine important in immune regulation, and TSLP dysregulation is associated with numerous diseases. TSLP is produced by many cell types, but has predominantly been characterized as a secreted factor from epithelial cells which activates dendritic cells (DC) that subsequently prime T helper (TH) 2 immunity. However, DC themselves make significant amounts of TSLP in response to microbial products, but the functional role of DC-derived TSLP remains unclear. We show that TSLPR signaling negatively regulates IL-1β production during dectin-1 stimulation of human DC. This regulatory mechanism functions by dampening Syk phosphorylation and is mediated via NADPH oxidase-derived ROS, HIF-1α and pro-IL-1β expression. Considering the profound effect TSLPR signaling has on the metabolic status and the secretome of dectin-1 stimulated DC, these data suggest that autocrine TSLPR signaling could have a fundamental role in modulating immunological effector responses at sites removed from epithelial cell production of TSLP."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2019.00921"xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Williams D.L."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Steinmetz M."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Goodall J.C."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Gaston J.S.H."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Cohen E.S."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Mallat Z."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Chee R."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Fitzmaurice T.J."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Webster S.J."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Elder M.J."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/author"Shaunak A.S.D."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/name"Front Immunol"xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/pages"921"xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/title"Dendritic Cell-Derived TSLP Negatively Regulates HIF-1alpha and IL-1beta During Dectin-1 Signaling."xsd:string
http://purl.uniprot.org/citations/31139177http://purl.uniprot.org/core/volume"10"xsd:string
http://purl.uniprot.org/citations/31139177http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31139177
http://purl.uniprot.org/citations/31139177http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31139177
http://purl.uniprot.org/uniprot/#_D0VY79-mappedCitation-31139177http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31139177
http://purl.uniprot.org/uniprot/#_A0A0C4DG43-mappedCitation-31139177http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31139177
http://purl.uniprot.org/uniprot/#_A0A510GAG5-mappedCitation-31139177http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31139177
http://purl.uniprot.org/uniprot/#_B2R617-mappedCitation-31139177http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31139177