RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/32973789http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32973789http://www.w3.org/2000/01/rdf-schema#comment"T cell exhaustion is an obstacle to immunotherapy for solid tumors. An understanding of the mechanism by which T cells develop this phenotype in solid tumors is needed. Here, hypoxia, a feature of the tumor microenvironment, causes T cell exhaustion (TExh) by inducing a mitochondrial defect. Upon exposure to hypoxia, activated T cells with a TExh phenotype are characterized by mitochondrial fragmentation, decreased ATP production, and decreased mitochondrial oxidative phosphorylation activity. The TExh phenotype is correlated with the downregulation of the mitochondrial fusion protein mitofusin 1 (MFN1) and upregulation of miR-24. Overexpression of miR-24 alters the transcription of many metabolism-related genes including its target genes MYC and fibroblast growth factor 11 (FGF11). Downregulation of MYC and FGF11 induces TExh differentiation, reduced ATP production and a loss of the mitochondrial mass in T cell receptor (TCR)-stimulated T cells. In addition, we determined that MYC regulates the transcription of FGF11 and MFN1. In nasopharyngeal carcinoma (NPC) tissues, the T cells exhibit an increased frequency of exhaustion and loss of mitochondrial mass. In addition, inhibition of miR-24 signaling decreases NPC xenograft growth in nude mice. Our findings reveal a mechanism for T cell exhaustion in the tumor environment and provide potential strategies that target mitochondrial metabolism for cancer immunotherapy."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.org/dc/terms/identifier"doi:10.3389/fimmu.2020.01906"xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"He J."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Gao S."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Zhang X.S."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Zhang C.X."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Huang D.J."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Chen H.X."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Gu J.M."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Liu Y.N."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Chen Q.Y."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Yang J.F."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Mai H.Q."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/author"Ni H.H."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/name"Front Immunol"xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/pages"1906"xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/title"Hypoxia Induces Mitochondrial Defect That Promotes T Cell Exhaustion in Tumor Microenvironment Through MYC-Regulated Pathways."xsd:string
http://purl.uniprot.org/citations/32973789http://purl.uniprot.org/core/volume"11"xsd:string
http://purl.uniprot.org/citations/32973789http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32973789
http://purl.uniprot.org/citations/32973789http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32973789
http://purl.uniprot.org/uniprot/#_A0A0B4J1R1-mappedCitation-32973789http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32973789