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Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RNA-Seq]

ABSTRACT: PD-L1 is a ligand for the inhibitory PD1 receptor on T cells and its expression in some cancers inhibits anti-cancer immune response. In melanoma, PD-L1 expression is induced in response to immune stimuli but in a proportion of melanomas it is constitutively expressed. Factors that drive constitutive expression of PD-L1 are unknown. Here we performed RNA-Seq analysis of six cell lines that constitutively express PD-L1 (PD-L1 positive, referred to as PD-L1CON) and six cell lines that only express PD-L1 after treatment with IFN- (PD-L1 negative, referred to as PD-L1IND)

ORGANISM(S): Homo sapiens

PROVIDER: GSE107620 | GEO | 2018/05/24

REPOSITORIES: GEO

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Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma [RRBS]

Project description:PD-L1 is a ligand for the inhibitory PD1 receptor on T cells and its expression in some cancers inhibits anti-cancer immune response. In melanoma, PD-L1 expression is induced in response to immune stimuli but in a proportion of melanomas it is constitutively expressed. Factors that drive constitutive expression of PD-L1 are unknown. Here we performed genome-scale methylation analysis of six cell lines that constitutively express PD-L1 (PD-L1 positive, referred to as PD-L1CON) and six cell lines that only express PD-L1 after treatment with IFN- (PD-L1 negative, referred to as PD-L1IND)

2018-05-24 | GSE107621 | GEO

Multiplex PRM quantitation of CD8a, CD4, LAG3, PD1, PD-L1 and PD-L2

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2018-10-04 | PXD011152 | Pride

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_RNA-seq]

Project description:BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We discovered that the maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. BETi directly repressed constitutively expressed and IFN-γ induced CD274 expression across different human and mouse tumor cell lines and primary patient samples. Mechanistically, BETi decreased Brd4 occupancy at the Cd274 locus without any change in Myc occupancy, resulting in transcriptional pausing and rapid loss of Cd274 mRNA production. Finally, targeted inhibition of the PD1/PD-L1 axis by combining anti-PD1 antibodies and the BETi JQ1 caused synergistic responses in mice bearing Myc-driven lymphomas. Our data uncovers a novel interaction between BETi and the PD-1/PD-L1 immune-checkpoint and provides novel insight into the transcriptional regulation of CD274.

2017-02-01 | GSE94133 | GEO

BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [EuMyc_ChIP-seq]

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BET-Bromodomain Inhibitors Engage The Host Immune System And Regulate Expression Of The Immune Checkpoint Ligand PD-L1 [3mRNA-seq]

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Supplementation with α-ketoglutarate improved the efficacy of anti-PD1 melanoma treatment through epigenetic modulation of PD-L1

Project description:Patients with advanced melanoma have shown an improved outlook after receiving anti-PD1 therapy, but the low response rate restricts clinical benefit; therefore, enhancing anti-PD1 therapy efficacy remains a major challenge. Here, our findings show significantly higher abundance of α-KG in healthy controls, anti-PD1-sensitive melanoma-bearing mice, and anti-PD1-sensitive melanoma patients; moreover, supplementation with α-KG enhanced the efficacy of anti-PD1 immunotherapy and increased PD-L1 expression in melanomas via STAT1/3. We also found that supplementation with α-KG significantly increased methylcytosine dioxygenase TET2/3, which led to an increased 5-hydroxymethylcytosine (5-hmC) level in the PD-L1 promoter. As a consequence, STAT1/3 had been recognized and stabilized in PD-L1 promoter to upregulate PD-L1 expression. Importantly, single-cell sequencing of preclinical samples and analysis of clinical data revealed that the TET2/3-STAT1/3-CD274 signaling was associated with sensitivity to anti-PD1 treatment in melanoma. Taken together, we provide a novel insight into α-KG's function in melanoma anti-PD1 treatment and supplement of α-KG is a novel promising strategy to improve the efficacy of anti-PD1 therapy.

2023-03-08 | GSE223110 | GEO

The PD-1/PD-L1 pathway maintains an immunosuppressive environment essential for neonatal heart regeneration [scRNA-seq]

Project description:The adult heart responds to injury by scarring with consequent loss of contractile function, whereas the neonatal heart possesses the ability to regenerate. We compared the immune response to injury in neonatal and adult mouse hearts and discovered that the PD1/PD-L1 immune checkpoint pathway is highly activated in regenerative hearts but is silenced in later life. Deletion of the PD1 receptor or inactivation of its PD-L1 ligand prevented regeneration of neonatal hearts after injury. Our findings reveal a previously unrecognized role of the PD1/PD-L1 pathway in the control of heart regeneration through modulating T cell activity and inflammation following injury and provide new inroads into the control of adult tissue regeneration.

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The PD-1/PD-L1 pathway maintains an immunosuppressive environment essential for neonatal heart regeneration [Spatial]

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Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

Project description:Global hypomethylation mediated changes regulate constitutive PD-L1 expression in melanoma

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Project description:PD-1 is constitutively expressed on a fraction of ILC3 in the gut. To identify the transcriptional differences between PD1+ and PD1- ILC3, we have sorted these subsets and analysed their transcriptional regulation by RNA-Seq.

2024-02-29 | GSE254794 | GEO

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