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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation [WGBS]

ABSTRACT: De novo DNA methylation establishes T cell exhaustion and inhibits PD-1 blockade-mediated T-cell rejuvenation.

ORGANISM(S): Mus musculus

PROVIDER: GSE99450 | GEO | 2017/06/30

SECONDARY ACCESSION(S): PRJNA388487

REPOSITORIES: GEO

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation [expression]

Project description:De novo DNA methylation establishes T cell exhaustion and inhibits PD-1 blockade-mediated T-cell rejuvenation. Expression profiling of chronically stimulated WT and Dnmt3a cKO antigen-specific CD8 T cells.

2017-06-30 | GSE99449 | GEO

De Novo Epigenetic Programs Inhibit PD-1 Blockade-Mediated T Cell Rejuvenation.

Project description: Not available

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation

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

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation

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Microarray data for rejuvenation experiments through reprogramming

Project description:Proliferative and replicative senescent fibroblasts from aged human donors were reprogrammed towards pluripotency and re-differentiated in fibroblasts and then further analyzed for rejuvenation assessment. Comparison of microarrays were performed by non hierarchical clustering visualized in with Treeview software

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Microarray data for rejuvenation experiments through reprogramming

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Cell Rejuvenation Signal Activations via Microfluidic Cell Stretch (passage 7)

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Role of de novo DNA methyltransferases in hematopoietic stem cells (WGBS)

Project description:To investigate the global DNA methylation changes in Dnmt3a-KO and Dnmt3ab-dKO HSCs compared to control HSCs, we performed whole genome bisulfite sequencing Mouse hematopoietic stem cell DNA methylation profiles of control, Dnmt3a-KO and Dnmt3ab-dKO HSCs were generated generated by deep sequencing, in duplicate, using Illumina Hiseq 2000

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Chronic Type I interferons signaling promotes lipid peroxidation-driven terminal CD8+T cell exhaustion and curtails anti-PD-1 treatment efficacy

Project description:Identifying signals that govern the differentiation of tumor-infiltrating CD8 + T cells (CD8 + TILs) towards exhaustion can improve current therapeutic approaches for cancer. Here, we show that type I interferons (IFN-Is) act as environmental cues enhancing terminal CD8 + T cell exhaustion in tumors. We found enrichment of IFNIs-stimulated genes (ISGs) within exhausted CD8 + T cells (Tex cells) in patients across various cancer types, with heightened ISG levels correlating with poor response to immune checkpoint blockade (ICB) therapy. In preclinical models, CD8 + TILs devoid of IFN-Is signaling developed less exhaustion features, provided better tumor control and showed greater response to ICB-mediated rejuvenation. Mechanistically, chronic IFN-Is stimulation perturbed lipid metabolism and redox balance in Tex cells, leading to aberrant lipid accumulation and elevated oxidative stress. Collectively, these defects promoted lipid peroxidation, which potentiated metabolic and functional exhaustion of Tex cells. Thus, cell intrinsic IFN-Is signaling regulates the extent of CD8+ TIL exhaustion, and has important implications for immunotherapy.

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