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http://purl.uniprot.org/citations/34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34813654http://www.w3.org/2000/01/rdf-schema#comment"T cells possess distinguishing effector functions and drive inflammatory disorders. We have previously identified IL-5-producing Th2 cells as the pathogenic population predominantly involved in the pathology of allergic inflammation. However, the cell-intrinsic signaling pathways that control the pathogenic Th2 cell function are still unclear. We herein report the high expression of acetyl-CoA carboxylase 1 (ACC1) in the pathogenic CD4+ T cell population in the lung and skin. The genetic deletion of CD4+ T cell-intrinsic ACC1 dampened eosinophilic and basophilic inflammation in the lung and skin by constraining IL-5 or IL-3 production. Mechanistically, ACC1-dependent fatty acid biosynthesis induces the pathogenic cytokine production of CD4+ T cells via metabolic reprogramming and the availability of acetyl-CoA for epigenetic regulation. We thus identified a distinct phenotype of the pathogenic T cell population in the lung and skin, and ACC1 was shown to be an essential regulator controlling the pathogenic function of these populations to promote type 2 inflammation."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.org/dc/terms/identifier"doi:10.1084/jem.20210639"xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Endo Y."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Nakayama T."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Ohara O."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Nakajima T."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Sasamoto S."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Yokoyama S."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Kanno T."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Tumes D.J."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/author"Asou H.K."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/name"J Exp Med"xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/pages"e20210639"xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/title"ACC1-expressing pathogenic T helper 2 cell populations facilitate lung and skin inflammation in mice."xsd:string
http://purl.uniprot.org/citations/34813654http://purl.uniprot.org/core/volume"218"xsd:string
http://purl.uniprot.org/citations/34813654http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34813654
http://purl.uniprot.org/citations/34813654http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34813654
http://purl.uniprot.org/uniprot/#_A0A0R4J1S9-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654
http://purl.uniprot.org/uniprot/#_Q9ESZ5-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654
http://purl.uniprot.org/uniprot/#_Q5SWU9-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654
http://purl.uniprot.org/uniprot/#_V9GXY1-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654
http://purl.uniprot.org/uniprot/#_V9GWR9-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654
http://purl.uniprot.org/uniprot/#_V9GWS0-mappedCitation-34813654http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34813654