RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/30049704http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30049704http://www.w3.org/2000/01/rdf-schema#comment"Group 2 innate lymphoid cells (ILC2s) are emerging as key players in the pathogenesis of allergic airway inflammation. The mechanisms regulating ILC2, however, are not fully understood. Here, we found that ICAM-1 is required for the development and function of ILC2. ICAM-1-deficient (ICAM-1-/- ) mice displayed significantly lower levels of ILC2s in the bone marrow and peripheral tissues than wild-type controls. CLP transfer and in vitro culture assays revealed that the regulation of ILC2 by ICAM-1 is cell intrinsic. Furthermore, ILC2s from ICAM-1-/- mice were functionally impaired, as indicated by the diminished production of type-2 cytokines in response to IL-33 challenge. The reduction in lung ILC2s caused a clear remission of airway inflammation in ICAM-1-/- mice after administration of papain or Alternaria alternata. We further demonstrate that ILC2 defects caused by ICAM-1 deficiency are due to ERK signaling-dependent down-regulation of GATA3 protein. Collectively, these observations identify ICAM-1 as a novel regulator of ILC2."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.org/dc/terms/identifier"doi:10.1084/jem.20172359"xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Zhou J."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Yang Q."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Shi K."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Xiao Q."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Liu Y.F."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Liu G.Y."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Wang H.K."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Guan Y.J."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Cai W.P."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Gabrilovich D.I."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/author"Lei A.H."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/name"J Exp Med"xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/pages"2157-2174"xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/title"ICAM-1 controls development and function of ILC2."xsd:string
http://purl.uniprot.org/citations/30049704http://purl.uniprot.org/core/volume"215"xsd:string
http://purl.uniprot.org/citations/30049704http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30049704
http://purl.uniprot.org/citations/30049704http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30049704
http://purl.uniprot.org/uniprot/#_B0QZX1-mappedCitation-30049704http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30049704
http://purl.uniprot.org/uniprot/#_P34902-mappedCitation-30049704http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30049704
http://purl.uniprot.org/uniprot/#_P13597-mappedCitation-30049704http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30049704