| http://purl.uniprot.org/citations/35917184 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35917184 | http://www.w3.org/2000/01/rdf-schema#comment | "Lysosomal acid lipase (LAL) is a key enzyme in the metabolic pathway of neutral lipids. In the blood of LAL-deficient (Lal-/-) mice, increased CD11c+ cells were accompanied by upregulated programmed cell death ligand 1 (PD-L1) expression. Single-cell RNA sequencing of Lal-/-CD11c+ cells identified 2 distinctive clusters with a major metabolic shift toward glucose utilization and reactive oxygen species overproduction. Pharmacologically blocking pyruvate dehydrogenase in glycolysis not only reduced CD11c+ cells and their PD-L1 expression but also reversed their capabilities of T cell suppression and tumor growth stimulation. Colony-stimulating factor 1 receptor (CSF1R) played an essential role in controlling Lal-/-CD11c+ cell homeostasis and function and PD-L1 expression. Pharmacological inhibition of LAL activity increased CD11c, PD-L1, and CSF1R levels in both normal murine myeloid cells and human blood cells. Tumor-bearing mice and human patients with non-small cell lung cancer also showed CD11c+ cell expansion with PD-L1 and CSF1R upregulation and immunosuppression. There were positive correlations among CD11c, PD-L1, and CSF1R expression and negative correlations with LAL expression in patients with lung cancer or melanoma using The Cancer Genome Atlas database and patient samples. Therefore, CD11c+ cells switched their functions to immune suppression and tumor growth stimulation through CSF1R/PD-L1 upregulation and metabolic reprogramming."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.org/dc/terms/identifier | "doi:10.1172/jci.insight.156623"xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Du H."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Liu S."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Ding X."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Singh K."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Wan J."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Yan C."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Zhao T."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Johnson E.M."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Sen C.K."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/author | "Hanna N.H."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/name | "JCI Insight"xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/pages | "e156623"xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/title | "Lysosomal acid lipase, CSF1R, and PD-L1 determine functions of CD11c+ myeloid-derived suppressor cells."xsd:string |
| http://purl.uniprot.org/citations/35917184 | http://purl.uniprot.org/core/volume | "7"xsd:string |
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