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Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [ATAC-seq]

ABSTRACT: Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [ATAC-seq]

PROVIDER: PRJNA801421 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17782800_1.fastq.gz	Fastqsanger.gz
	SRR17782800_2.fastq.gz	Fastqsanger.gz
	SRR17782801_1.fastq.gz	Fastqsanger.gz
	SRR17782801_2.fastq.gz	Fastqsanger.gz
	SRR17782802_1.fastq.gz	Fastqsanger.gz

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Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells

Project description:Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells

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Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [ATAC-seq]

Project description:While inhibition of T cell co-inhibitory receptors has revolutionized cancer therapy, the mechanisms governing their expression on human T cells have not been elucidated. Type 1 interferon (IFN-I) modulates T cell immunity in viral infection, autoimmunity, and cancer, and may facilitate induction of T cell exhaustion in chronic viral infection. Here we show that IFN-I regulates co-inhibitory receptor expression on human T cells, inducing PD-1/TIM-3/LAG-3 while surprisingly inhibiting TIGIT expression. High-temporal-resolution mRNA profiling of IFN-I responses enabled the construction of dynamic transcriptional regulatory networks uncovering three temporal transcriptional waves. Perturbation of key transcription factors on human primary T cells revealed unique regulators that control expression of co-inhibitory receptors. We found that the dynamic IFN-I response in vitro closely mirrored T cell features with IFN-I linked acute SARS-CoV-2 infection in human, with high LAG3 and decreased TIGIT expression. Finally, our gene regulatory network identified SP140 as a key regulator for differential LAG3 and TIGIT expression, which were validated at the level of protein expression. The construction of IFN-I regulatory networks with identification of unique transcription factors controlling co-inhibitory receptor expression may provide targets for enhancement of immunotherapy in cancer, infectious diseases, and autoimmunity.

2022-01-31 | GSE195540 | GEO

Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [Kinetics RNA-seq]

Project description:Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [Kinetics RNA-seq]

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Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [shRNA RNA-seq]

Project description:Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [shRNA RNA-seq]

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Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [shRNA RNA-seq]

2022-01-31 | GSE195542 | GEO

Type I Interferon Transcriptional Network Regulates Expression of Coinhibitory Receptors in Human T cells [Kinetics RNA-seq]

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Tumor Interferon Signaling Regulates a Multigenic Resistance Program to Immune Checkpoint Blockade [ATAC-Seq]

Project description:The goal of this study is to investigate if interferon signaling regulates immune checkpoint blockade in mouse melanoma model.

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Pbrm1 regulates interferon signaling in mouse AML

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Long noncoding RNA INCA1 regulates tumor interferon signaling

Project description:Tumor interferon signaling regulates the expression of immunosuppressive molecules and promotes cancer immune evasion. Although the role of long noncoding RNAs (lncRNAs) in the regulation of gene expression is now emerging, their function in tumor interferon signaling remains unexplored. We have identified the interferon-γ (IFNγ)-stimulated non-coding RNA 1 (INCA1) as a novel lncRNA expressed form the PD-L1 locus. INCA1 is expressed in multiple tumor types and its levels increase after IFNγ stimulation. In this study we performed transcriptome analysis (RNA-seq) of INCA1 knockdown cells and show that INCA1 regulates the expression of several interferon-stimulated genes. Overall, our findings reveal INCA1 as a critical component of the tumor interferon signaling.

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Stat1 activation, through systemic interferon signaling, and upregulation of innate immune system receptors drives inflammaging, that is ameliorated by dietary restriction intervention [ATAC-seq]

Project description:Aging is the result of an accumulation of molecular damages, driven by multiple factors like metabolic and oxidative stress, (epi)genetic alterations, and microbiome dysbiosis. In addition, aging is characterized by a chronic, low-grade inflammation known as inflammaging that represents a high significant risk factor for most, if not all, age-related diseases. Dietary restriction (DR) is the best-known non-invasive method to ameliorate the aging phenotype in many organisms. While it has been shown that DR reduces the inflammation in some tissues, the molecular mechanisms in old individuals are still largely unknown. Here we identify a multi-tissue gene network which regulates the inflammaging and that is ameliorated by DR. Using transcriptional profiling (RNA-seq), we found that aging upregulates the innate immune system receptor together with the activation of a systemic interferon (IFN) signaling through the Interferon Regulatory Factors (Irf), inflammatory cytokines and finally Stat1 transcription factor. Our results suggest that DR is able to ameliorate inflammaging by downregulating the expression and the activity of almost all the components of this gene network. In addition, chromatin accessibility genome-wide analysis showed that the binding site of Irf and Stat1 in the promoter of their target genes are more open in aging and become closer upon DR treatment indicating a transcriptional control of the inflammaging phenotype involving epigenetic modifications. Our results provide a comprehensive understanding of the molecular network regulating the inflammation in aging and DR and present novel anti-inflammaging therapeutic targets.

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