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Gene expression of PD-L1 high and low pancreatic beta cells, after 20h of incubation wiht 50pg.mL of IFNγ.

ABSTRACT: Characterization of FACS-sorted PD-L1 high and low mouse pancreatic beta cells after 20h of incubation with low dose of IFNγ.

ORGANISM(S): Mus musculus

PROVIDER: GSE221078 | GEO | 2023/01/11

REPOSITORIES: GEO

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Gene expression of PD-L1 high and low pancreatic beta cells, after 20h of incubation wiht 50pg.mL of IFNγ.

Project description:Gene expression of PD-L1 high and low pancreatic beta cells, after 20h of incubation wiht 50pg.mL of IFNγ.

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IFNγ treatment restores TAP-dependent presentation competence of PD-L1 sensitive PDAC cells

Project description:For immunotherapy, there is an urgent need to restore presentation-competence of cancer cells with defects in MHC-I processing/presentation. We identified two tumor-specific antigens expressed in the ER of pancreatic ductal adenocarcinoma cells (PDACCs) that induced effector CD8 T cells either independent (Cripto-1-Kb/Cr16-24) or dependent (gp70-Kb/p15E) on TAP-mediated antigen processing/presentation by DNA immunization. In systematic analyses, we showed that transplantation into syngeneic C57BL/6J mice or IFNγ-treatment in vitro upregulated MHC-I but also co-inhibitory PD-L1 molecules on PDACCs. IFNγ-treated PDACCs efficiently formed solid tumors in transplanted C57BL/6J and PD-L1-/- but were rejected in PD-1-/- mice. PDACCs induced a prophylactic immunity against tumor transplants in C57BL/6J mice when irradiated at day 2-3 post IFNγ-treatment, thereby silencing the tumor-initiated immune-suppressive PD-L1/PD-1-signaling axis. Immune-protection correlated with a significant enhanced induction of CD8 T cells against the TAP- but not the TAP-dependent antigen/epitope.

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Gene expression data from NK cells sorted for PD-L1 after co-incubation with K562 myeloid leukemia cells

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PD-L1 mediates IFNγ-regulation of glucose but not of tryptophan metabolism in clear cell renal cell carcinoma

Project description:The immune checkpoint programmed death-ligand 1 (PD-L1) is expressed on the cell surface of tumor cells and is key for maintaining an immunosuppressive microenvironment through its interaction with the programmed death 1 (PD-1). Clear cell renal cell carcinoma (ccRCC) is a highly immunogenic cancer characterized by an aberrant aerobic glycolytic metabolism and is known to overexpress PD-L1. Multiple immunotherapies have been approved for the treatment of ccRCC, including cytokines and immune checkpoint inhibitors. Recently the intrinsic role of PD-L1 and interferon gamma (IFNγ) signaling have been studied in several types of tumor cells, yet it remains unclear how they affect the metabolism and signaling pathways of ccRCC. Using metabolomics, metabolic assays and RNAseq, we showed that IFNγ enhanced aerobic glycolysis and tryptophan metabolism in ccRCC cells in vitro and induced the transcriptional expression of signaling pathways related to inflammation, cell proliferation and cellular energetics. These metabolic and transcriptional effects were partially reversed following transient PD-L1 silencing. Aerobic glycolysis, as well as signaling pathways related to inflammation, were not induced by IFNγ when PD-L1 was silenced, however, tryptophan metabolism and activation of Jak2 and STAT1 were maintained. Our data demonstrate that PD-L1 expression is required to mediate some of IFNγ’s effect in ccRCC cells and highlight the importance of PD-L1 signaling in regulating the metabolism of ccRCC cells in response to inflammatory signals.

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Project description:Blocking the PD-1/PD-L1 immunosuppressive pathway has shown promise in the treatment of certain cancers including melanoma. This study investigates differences in the gene expression profiles of human melanomas that do or do not display the immunosuppressive protein PD-L1. Further understanding of genes expressed within the tumor microenvironment of PD-L1+ tumors may lead to improved rationally designed treatments. Gene expression profiling was performed on total RNA extracted by laser capture microdissection from 11 archived formalin-fixed paraffin-embedded (FFPE) melanoma specimens, 5 of which were PD-L1 positive and 6 PD-L1 negative. Details of the design, and the gene signatures found are given in the paper associated with this GEO Series: Janis M. Taube, Geoffrey D. Young, Tracee L. McMiller, Shuming Chen, January T. Salas, Theresa S. Pritchard, Haiying Xu, Alan K. Meeker, Jinshui Fan, Chris Cheadle, Alan E. Berger, Drew M. Pardoll, and Suzanne L. Topalian, Differential expression of immune-regulatory genes associated with PD-L1 display in melanoma: implications for PD-1 pathway blockade, Clin Cancer Res 2015, in press.

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Project description:Checkpoint inhibitors like anti-PD1/PD-L1 have demonstrated significant therapeutic efficacy in a subset of patients partly through reinvigoration of CD8 T cells. However, their impact on myeloid cells remains largely unknown. Here we report that anti-PD-L1 treatment favorably impacts the phenotype and function of tumor macrophages by polarizing the macrophage compartment towards a more pro-inflammatory phenotype. This phenotype was characterized by a decrease in Arginase-I (ARG1) expression and an increase in iNOS, MHCII, and CD40 expression. Whole-transcriptome profiling further confirmed extensive polarization of both tumor monocytes and macrophages from a suppressive to a pro-inflammatory, immuno-stimulatory phenotype. This polarization was driven mainly through IFNγ and was associated with enhanced T cell activity. Transfer of monocytes into anti-PD-L1-treated tumor-bearing mice led to macrophage differentiation into a more pro-inflammatory phenotype, with an increase in CD8 T cells expressing granzyme B and an increase in the CD8/Treg ratio compared to control-treated mice. While in responsive tumor models anti-PD-L1 treatment remodeled the macrophage compartment with beneficial effects on T cells, both macrophage reprogramming and depletion were needed to maximize anti-PD-L1 responses in a tumor immune contexture with high macrophage burden. Our results demonstrate that anti-PD-L1 treatment can favorably remodel the macrophage compartment in responsive tumor models towards a more pro-inflammatory phenotype, mainly through increased IFNγ levels. They also suggest that directly targeting these cells with reprogramming and depleting agents may further augment the breadth and depth of response to anti-PD-L1 treatment in less responsive or more macrophage-dense tumor microenvironments. The "SAMPLE_ID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is NGS1772.

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