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http://purl.uniprot.org/citations/29336888http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29336888http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29336888http://www.w3.org/2000/01/rdf-schema#comment"Therapeutic harnessing of adaptive immunity via checkpoint inhibition has transformed the treatment of many cancers. Despite unprecedented long-term responses, most patients do not respond to these therapies. Immunotherapy non-responders often harbor high levels of circulating myeloid-derived suppressor cells (MDSCs)-an immunosuppressive innate cell population. Through genetic and pharmacological approaches, we uncovered a pathway governing MDSC abundance in multiple cancer types. Therapeutic liver-X nuclear receptor (LXR) agonism reduced MDSC abundance in murine models and in patients treated in a first-in-human dose escalation phase 1 trial. MDSC depletion was associated with activation of cytotoxic T lymphocyte (CTL) responses in mice and patients. The LXR transcriptional target ApoE mediated these effects in mice, where LXR/ApoE activation therapy elicited robust anti-tumor responses and also enhanced T cell activation during various immune-based therapies. We implicate the LXR/ApoE axis in the regulation of innate immune suppression and as a target for enhancing the efficacy of cancer immunotherapy in patients."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2017.12.026"xsd:string
http://purl.uniprot.org/citations/29336888http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2017.12.026"xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Takeda S."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Takeda S."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Zhao C."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Zhao C."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Kurth I."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Kurth I."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Mita M."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Mita M."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Andreu-Agullo C."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Andreu-Agullo C."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Tavazoie S.F."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Tavazoie S.F."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Mita A."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Mita A."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Chmielowski B."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Chmielowski B."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Derbyshire M.L."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Derbyshire M.L."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Gonsalves F.C."xsd:string
http://purl.uniprot.org/citations/29336888http://purl.uniprot.org/core/author"Gonsalves F.C."xsd:string