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http://purl.uniprot.org/citations/36941554http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36941554http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

The combined application of immune checkpoint inhibitors (ICIs) and anti-angiogenesis therapy has shown synergistic effects on glioblastoma (GBM). As important resources of PD-L1 in the tumor microenvironment (TME), tumor-associated macrophages (TAMs) have significant impact of the efficiency of ICIs. However, the effects of anti-angiogenesis agents on immune checkpoints expression are not fully understood.

Method

GBM-educated macrophages were generated from circulating monocytes of healthy controls and GBM patients under the education of GBM cell line. Surface expression of PD-L1 and VEGFR1 on GBM-educated macrophages was analyzed. VEGFR1 NAb and soluble VEGFR1 (sVEGFR1) were added and their effects on PD-L1 expression on TAMs was investigated. Serum soluble PD-L1 (sPD-L1) and sVEGFR1 levels in GBM patients were measured and their correlation was analyzed.

Result

The expression intensity of PD-L1 on GBM-educated macrophages was higher and its up-regulation partially depends on VEGFR1 signaling pathway. GBM-educated macrophages secreted less levels of soluble VEGFR1 (sVEGFR1), and exogenous sVEGFR1 down-regulated PD-L1 expression intensity. PD-L1 blockade promoted the secretion of sVEGFR1. Finally, sVEGFR1 and sPD-L1 in serum of GBM patients were overexpressed, and a positive correlation was found.

Conclusion

These findings reveal the interaction between PD-L1 and VEGFR1 signaling pathway in GBM-educated macrophages. VEGFR1 is involved with PD-L1 overexpression, which can be impeded by autocrine regulation of sVEGFR1. sVEGFR1 secretion by GBM-educated macrophages can be promoted by PD-L1 blockade. Taken together, these findings provide evidences for the combined application of ICIs and anti-angiogenesis therapies in the treatment of GBM."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.org/dc/terms/identifier"doi:10.1186/s12885-023-10733-5"xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/author"Li Z."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/author"Sun J."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/author"Zhang Z."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/name"BMC Cancer"xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/pages"259"xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/title"Interaction between PD-L1 and soluble VEGFR1 in glioblastoma-educated macrophages."xsd:string
http://purl.uniprot.org/citations/36941554http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/36941554http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/36941554
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