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Specific induction of GPR15 expression in heterogeneous blood lymphocytes by smoking

ABSTRACT: Specific induction of GPR15 expression in heterogeneous blood lymphocytes by smoking

PROVIDER: PRJNA472789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7208391_1.fastq.gz	Fastqsanger.gz
	SRR7208391_2.fastq.gz	Fastqsanger.gz
	SRR7208392_1.fastq.gz	Fastqsanger.gz
	SRR7208392_2.fastq.gz	Fastqsanger.gz

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Specific induction of GPR15 expression in heterogeneous blood lymphocytes by smoking

Project description:Although a mucosal and cutaneous chemokine ligand for G protein –linked receptor GPR15 was recently identified, the physiological role of GPR15 remains yet elusive. In blood, in has been shown that smoking is, to date, the only specific condition leading to an increase in GPR15+ T cells. We therefore used transcriptome sequencing to describe GPR15-expressing blood T cells in more detail.

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Smoking induced expression of the GPR15 gene indicates its potential role in chronic inflammatory pathologies

Project description:The aim of present study was to study the changes in peripheral blood gene expression profile induced by smoking. RNA was extracted from the PBMCs of 48 persons with detailed smoking history (24 were non-smokers, 16 were current smokers and 8 were ex-smokers). Gene expression profile was evaluated with the RNA sequencing and results were analyzed separately in males (24) and females (24). In male smokers, 13 genes were statistically significantly (FDR < 0.1) differentially expressed. In female smoker, 5 genes were differentially expressed with the FDR<0.1. Most of the differentially expressed genes were different between male and female smokers. However, GPR15, expression was changed in male and female smokers compared to non-smokers. Further analysis on the methylation of the genes GPR15 identified significant hypomethylation in smokers compared to non-smokers. GPR15 is the chemo-attractant receptor that regulates T-cell migration and immunity. Up-regulation of GPR15 could explain to some extend the health hazards of smoking for chronic inflammatory diseases

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Ahr-Foxp3-RORγt Axis Controls Gut Homing of CD4+ T Cells by Regulating GPR15

Project description:The orphan chemoattractant receptor GPR15 is important for homing T lymphocytes to the large intestine, thereby maintaining intestinal immune homeostasis. However, the molecular mechanisms underlying the regulation of GPR15 expression remain elusive. Here we show a central role of the aryl hydrocarbon receptor (Ahr) in promoting GPR15 expression both in mice and human, thus gut homing of T lymphocytes. Mechanistically, Ahr directly binds to open chromatin regions of the Gpr15 locus to enhance its expression. Ahr transcriptional activity in directing GPR15 expression was modulated by two transcription factors, Foxp3 and RORγt, both of which are expressed preferentially by gut Tregs in vivo. Specifically, Foxp3 interacted with Ahr and enhanced Ahr DNA binding at the Gpr15 locus, thereby promoting GPR15 expression. In contrast, RORγt plays an inhibitory role at least in part by competing with Ahr binding to the Gpr15 locus. Our findings thus demonstrate a key role for Ahr in regulating Treg intestinal homing under the steady state and during inflammation, and the importance of Ahr-RORγt-Foxp3 axis in regulating gut homing receptor GPR15 expression by lymphocytes.

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Project description:GPR15 is an orphan G-protein coupled receptor and its expression is abundant among T cells in the large intestine lamina propria. We used microarrays to examine charateristics of GPR15- vs GPR15+ CD4+ T cells in LILP and identified distinct classes of up-regulated genes in GPR15+ CD4+ T cells. We have generated GFP knock-in mice in GPR15 locus and used GFP as a maker for GPR15 expression. In heterozygous mice, GPR15+CD4+ T cells and GPR15-CD4-T cells were sorted and RNA was prepared from them.

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Project description:GPR15+ vs GPR15- tumor-associated Tregs

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Expression data from GPR15+CD4+ and GPR15-CD4+ T cells in LILP

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