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ATACseq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

ABSTRACT: ATACseq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

PROVIDER: PRJEB46379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6318310_1.fastq.gz	Fastqsanger.gz
	ERR6318310_2.fastq.gz	Fastqsanger.gz
	ERR6318311_1.fastq.gz	Fastqsanger.gz
	ERR6318311_2.fastq.gz	Fastqsanger.gz
	ERR6318312_1.fastq.gz	Fastqsanger.gz

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ChIP seq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

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ATACseq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

Project description:To investigate how chromatin is shaped during inflammation geared towards the development of fibrosis in peritoneal tissue, we performed ATAC-seq in peritoneal membranes from wt and Il-6 knockout mice challenged with SES (a lyophilized cell-free supernatant prepared from Staphylococcus epidermidis ) together with Th1 polarised CD4+ T-cells administered via the intraperitoneal route. Peritoneal membrane was harvested 3 hours after injection, immediately snap-frozen in liquid nitrogen, and stored at -80C until processed. Tissues were diced and ground to a fine powder with intermittent addition of liquid nitrogen and Omni-ATAC-seq was performed.

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ChIP seq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

Project description:Using ChIP-Seq analysis we explore regulation of gene expression changes during inflammatory peritonitis induced by challenge with bacterial ligands administered via the intra-peritoneal route. A resuspended lypholised supernatant of Staphylococcus epidermidis (SES) was administered with or without ex vivo generated CD4+ T-cells (Th1-polarised) to understand the role of adaptive immune responses in shaping inflammatory processes. To study the role of Signal transducer and Activator of Transcription 1 and 3 (STAT1/STAT3) we performed ChIP-seq on peritoneal membrane sections isolated from wt and Il-6 knockout mice three hours post-challenge. Membrane sections were snap frozen in liquid nitrogen prior to downstream processing using established ChIP-seq protocols (Illumina Truseq).

2022-04-04 | E-MTAB-10758 | biostudies-arrayexpress

RNA-seq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

Project description:To investigate potential changes in the provision of competent host defence versus inflammation-induced tissue injury, we used RNA-seq to profile gene signatures in ‘resolving’ and ‘pro-fibrotic’ peritoneal lining tissues. We performed RNA-seq in peritoneal membranes from WT and IL6KO mice challenge with SES - Lyophilized cell-free supernatant prepared from Staphylococcus epidermidis ('resolving') and mice challenged with SES and CD4+ Th1 cells at the same time ('pro-fibrotic'). The peritoneal membrane was harvested at 3h and 6h after the injection.

2022-04-04 | E-MTAB-10087 | biostudies-arrayexpress

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Project description:RNA-seq: STAT1 and STAT3 transcription factors sense and interpret changes in inflammation through engagement of specific enhancers

2023-06-15 | E-MTAB-10087 | ExpressionAtlas

Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [ATACseq]

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Project description:STAT1 plays a cental role in the induction of interferon-stimulated genes, but interferon alpha can activate a STAT1-independent pathway that leads to gene expression. We performed microarray analysis to examine whether like interferon alpha, interferon lambda, a newly discovered interferon, can induce the expression of interferon-stimulated genes in the absence of STAT1. Control and STAT1 knockout Huh-7.5 hepatoma cells were left untreated or treated with 1000 U/ml of human interferon alpha 2a or interferon lambda 1 (PBL) for 24 h, and total RNA was extracted. Sense-strand DNA was generated from 200 ng of total RNA, fragmented, and labeled using a GeneChip WT Plus Reagent Kit (Affymetrix). Six samples were obtained and each sample was anlyzed using one GeneChip.

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Project description:ATACseq data for this study.

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Antitumor progenitor exhausted CD8 T cells are sustained with TCR engagement [ATACseq]

Project description:Durability of an antitumor immune response is mediated in part by the persistence of progenitor exhausted CD8 T cells (Tpex). Tpex serve as a source for the pool of effector T cells, and in the absence of their cognate antigen, they are able to preserve their quantity through a process of self-renewal. However, it remains unknown how TCR engagement impacts the self-renewal capacity of Tpex in settings of continued antigen exposure. Here, we used a Lewis lung carcinoma model that elicits an optimal or attenuated TCR signal in CD8 T cells to investigate its effect on Tpex persistence during tumor development. Longitudinal phenotyping and single-cell transcriptomics of tumor-specific T cells revealed that formation of the Tpex reservoir in tumor-draining lymph nodes, and its subsequent replenishment of intratumoral Tpex, is dependent on optimal TCR engagement. Notably, adoptive transfer of optimally primed Tpex into a tumor setting with attenuated TCR stimulation significantly accelerates their terminal differentiation, contrasting to the sustained self-renewal occuring with optimal TCR stimulation. This TCR-reinforced Tpex development and self-renewal is coupled to proximal positioning to dendritic cell niches and epigenetic imprinting that involves increased chromatin accessibility at Egr2 and Tcf1 target loci. Collectively, our study highlights the critical role of TCR engagement in sustaining Tpex during tumor progression

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