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http://purl.uniprot.org/citations/28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28300057http://www.w3.org/2000/01/rdf-schema#comment"Toll-like receptors (TLRs) are located either on the cell surface or intracellularly in endosomes and their activation normally contributes to the induction of protective immune responses. However, in cancer their activation by endogenous ligands can modulate tumour progression. It is currently unknown how endosomal TLRs regulate endogenous anti-tumour immunity. Here we show that TLR3, 7 and 9 deficiencies on host cells, after initial tumour growth, result in complete tumour regression and induction of anti-tumour immunity. Tumour regression requires the combined absence of all three receptors, is dependent on both CD4 and CD8 T cells and protects the mice from subsequent tumour challenge. While tumours in control mice are infiltrated by higher numbers of regulatory T cells, tumour regression in TLR-deficient mice is paralleled by altered vascular structure and strongly induced influx of cytotoxic and cytokine-producing effector T cells. Thus, endosomal TLRs may represent a molecular link between the inflamed tumour cell phenotype, anti-tumour immunity and the regulation of T-cell activation."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.org/dc/terms/identifier"doi:10.1038/ncomms14600"xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Lang S."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Dittmer U."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Moses K."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Klein J.C."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Buer J."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Brandau S."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Kirschning C.J."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Zelinskyy G."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Helfrich I."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/author"Sody S."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/pages"14600"xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/title"Combined toll-like receptor 3/7/9 deficiency on host cells results in T-cell-dependent control of tumour growth."xsd:string
http://purl.uniprot.org/citations/28300057http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/28300057http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28300057
http://purl.uniprot.org/citations/28300057http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28300057
http://purl.uniprot.org/uniprot/#_A0A1B0GTA2-mappedCitation-28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28300057
http://purl.uniprot.org/uniprot/#_A0A1Y7VI41-mappedCitation-28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28300057
http://purl.uniprot.org/uniprot/#_A0A1B0GS40-mappedCitation-28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28300057
http://purl.uniprot.org/uniprot/#_A0A1B0GSY9-mappedCitation-28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28300057
http://purl.uniprot.org/uniprot/#_A2AHJ1-mappedCitation-28300057http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28300057