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The Aryl Hydrocarbon Receptor Cell-Intrinsically Promotes Resident Memory CD8+ T Cell Differentiation and Function

ABSTRACT: The Aryl Hydrocarbon Receptor Cell-Intrinsically Promotes Resident Memory CD8+ T Cell Differentiation and Function

PROVIDER: PRJNA912138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22731200.fastq.gz	Fastqsanger.gz
	SRR22731187_1.fastq.gz	Fastqsanger.gz
	SRR22731187_2.fastq.gz	Fastqsanger.gz
	SRR22731188_1.fastq.gz	Fastqsanger.gz
	SRR22731188_2.fastq.gz	Fastqsanger.gz

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The Aryl Hydrocarbon Receptor Cell-Intrinsically Promotes Resident Memory CD8+ T Cell Differentiation and Function

Project description:The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4+ T cells; however, the cell-intrinsic role of Ahr in CD8+ T cells, remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8+ T cell (TRM) differentiation and function. Under steady state conditions or in an oral infection model, genetic ablation of Ahr in CD8+ T cells leads to an increase in CD127–KLRG1+ short lived effector cells (TSLE) and CD44+CD62L+ T central memory (TCM) cells, but a reduction in Granzyme B-producing CD69+CD103+ T resident memory (TRM) cells. Genome-wide transcriptome and cistrome analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8+ T cell population dependent on Ahr is revealed by single cell RNA-Seq, and deletion of Ahr in CD8+ T cells compromises anti-tumor immunity. Consistent with mouse, human IEL CD8+ T cells highly express AHR that regulates in vitro TRM differentiation and Granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8+ T cell immunity.

2023-01-11 | GSE220944 | GEO

The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

Project description:This SuperSeries is composed of the following subset Series: GSE15857: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Kidney GSE15858: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Liver Refer to individual Series

2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

Aryl hydrocarbon receptor dynamically regulates inflammatory and secretory gene pathways in decidual endometrial stromal cells

Project description:We report sequencing of chromatin immunoprecipitated DNA (ChIP-Seq) of Aryl Hydrocarbon Receptor (AHR) targets from decidual stromal cells with kynurenine treatment and normal decidualization media

2019-06-01 | GSE118413 | GEO

Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

Project description:Zebrafish larvae aryl hydrocarbon receptor ligands and inhibitor

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Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.

2010-09-05 | E-GEOD-19411 | biostudies-arrayexpress

The Aryl hydrocarbon receptor and FOS mediated cytotoxicity induced by Acenatobacter baumannii

Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.

2024-08-05 | PXD053768 | Pride

Aryl hydrocarbon receptor dynamically regulates immunological and secretory gene pathways in decidual endometrial stromal cells

Project description:We report mRNA sequencing from decidual stromal cells after 24 hours and 6 days treatment with Aryl Hydrocarbon Receptor (AHR) activators 100 µM L-kynurenine or 10 nM TCDD (2,3,7,8-Tetrachlorodibenzo-p-dioxin)

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Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

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Aryl Hydrocarbon Receptor deficiency influences B cell response

Project description:The aryl hydrocarbon receptor (AhR), a transcription factor known for mediating xenobiotic toxicity, is expressed in B cells, which are known targets for environmental pollutants. However, it is unclear what the physiological functions of AhR in B cells are. We show here that expression of Ahr in B cells is up-regulated upon B cell receptor (BCR) engagement and IL-4 treatment. Addition of a natural ligand of AhR, FICZ, induces AhR translocation to the nucleus and transcription of the AhR target gene Cyp1a1, showing that the AhR pathway is functional in B cells. AhR-deficient (Ahr-/-) B cells proliferate less than AhR-sufficient (Ahr+/+) cells following in vitro BCR stimulation and in vivo adoptive transfer models confirmed that Ahr-/- B cells are outcompeted by Ahr+/+ cells. Transcriptome comparison of AhR-deficient and sufficient B cells identified cyclin O (Ccno), a direct target of AhR, as a top candidate affected by AhR deficiency.

2016-11-16 | GSE86521 | GEO

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