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

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

PROVIDER: PRJNA854641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19909852.fastq.gz	Fastqsanger.gz
	SRR19909853.fastq.gz	Fastqsanger.gz
	SRR19909854.fastq.gz	Fastqsanger.gz
	SRR19909855.fastq.gz	Fastqsanger.gz
	SRR19909856.fastq.gz	Fastqsanger.gz

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

Project description:The PD-1/PD-L1 pathway maintains an immunosuppressive environment essential for neonatal heart regeneration

| PRJNA854636 | ENA

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

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

| PRJNA854163 | ENA

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

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.

2023-06-01 | GSE207215 | GEO

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

2023-06-01 | GSE207289 | GEO

Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

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.

2015-05-01 | E-GEOD-65041 | biostudies-arrayexpress

Expression data in PD-L1 positive and PD-L1 negative human melanoma samples

2015-05-01 | GSE65041 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-01 | GSE207290 | GEO

MLLT6 maintains PD‐L1 expression and mediates tumor immune resistance

Project description:MLLT6 maintains PD‐L1 expression and mediates tumor immune resistance

| PRJNA603767 | ENA

ACE2 Enhances Sensitivity to PD-L1 Blockade by Inhibiting Macrophage-Induced Immunosuppression and Angiogenesis [RNA-seq, anti-PD-L1 therapy]

Project description:Anti-PD-L1-based combination immunotherapy has become the first-line treatment for unresectable hepatocellular carcinoma (HCC). However, the objective response rate is lower than 40%, highlighting the need to identify mechanisms of tolerance to immune checkpoint inhibitors and accurate biomarkers of response. Here, we employed next-generation sequencing to analyze HCC samples from 10 patients receiving anti-PD-L1 therapy. Activation of the renin-angiotensin system was elevated in nonresponders compared with responders, and ACE2 expression was significantly downregulated in nonresponders. ACE2 deficiency promoted HCC development and anti-PD-L1 resistance, whereas ACE2 overexpression inhibited HCC progression in immune competent mice. Mass cytometry by time of flight (CyTOF) revealed that ACE2 deficient murine orthotopic tumor tissues featured elevated M2-like tumor-associated macrophages (TAMs), displayed a CCR5+PD-L1+ immunosuppressive phenotype, and exhibited high VEGFα expression. ACE2 downregulated tumor intrinsic CCL5 expression by suppressing NF-κB signaling through the ACE2/angiotensin-(1–7)/Mas receptor axis. The lower CCL5 levels led to reduced activation of the JAK-STAT3 pathway and suppressed PD-L1 and VEGFα expression in macrophages, blocking macrophage infiltration and M2-like polarization. Pharmacological targeting of CCR5 using maraviroc enhanced the tumor suppressive effect of anti-PD-L1 therapy. Together, these findings suggest that activation of the ACE2 axis overcomes the immunosuppressive microenvironment of HCC and may serve as an immunotherapeutic target and predictive biomarker of response to PD-L1 blockade.

2024-10-22 | GSE279750 | GEO

Gene-expression profiles of PD-L1-affected CD8+ T cells

Project description:Programmed cell death 1 ligand 1 (PD-L1) is known to suppress immune system and to be an unfavorable prognostic factor in ovarian cancer. The purpose of this study was to elucidate the function of PD-L1 in peritoneal dissemination. Tumor cell lysis by CTLs was attenuated when PD-L1 on tumor cells was overexpressed and promoted when it was silenced. PD-L1 overexpression also inhibited gathering and degranulation of CTLs. Gene expression profile of mouse CTLs caused by PD-L1-overexpressing ovarian cancer was related to human CTLs exhaustion. In mouse ovarian cancer dissemination models, depleting PD-L1 expression on tumor cells resulted in inhibited tumor growth in the peritoneal cavity and prolonged survival. Restoring immune function by inhibiting immune-suppressive factors such as PD-L1 may be a promising therapeutic strategy for peritoneal dissemination. Genome-wide transcriptional changes in OT-1 mouse CD8+ T cells that were co-incubated with OVA peptide-loaded ID8 mouse ovarian cancer cell lines. CTLs from 4 mice were devided into 2 groups, and co-incubated with PD-L1-overexpressed ID8 or PD-L1-depleted ID8.

2012-07-09 | E-GEOD-39205 | biostudies-arrayexpress

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