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The IL-33/ST2 axis and tissue Treg maintains epithelial homeostasis in the skin and restrains cancer development

ABSTRACT: The IL-33/ST2 axis and tissue Treg maintains epithelial homeostasis in the skin and restrains cancer development

PROVIDER: PRJNA1006323 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25663140_1.fastq.gz	Fastqsanger.gz
	SRR25663140_2.fastq.gz	Fastqsanger.gz
	SRR25663141_1.fastq.gz	Fastqsanger.gz
	SRR25663141_2.fastq.gz	Fastqsanger.gz
	SRR25663142_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The IL-33/ST2 axis and tissue Treg maintains epithelial homeostasis in the skin and restrains cancer development

Project description:IL-33 is constitutively expressed in many epithelial tissues at steady state and signals through the receptor, ST2. IL-33 is released upon tissue injury and functions as an endogenous danger signal to alert the immune system to tissue damage. Here we investigate the physiological role of the IL-33/ST2 axis in skin homeostasis and cancer development. We show that expression of IL-33 differentiates malignant from normal/benign human tissues and that in mouse models of cutaneous squamous cell carcinoma the IL-33/ST2 axis protects against carcinogenesis. Tissue Treg are the predominant cells expressing ST2 in the skin and localise around the hair follicle and IL-33+ epithelial cells (EC). Adoptive transfer experiments demonstrate that skin Treg regulate EC differentiation, minimizes mutational load and retrains cancer development following exposure to an environmental carcinogen. Our findings indicate an important role for direct EC-Treg cross-talk as an early checkpoint to contain tissue damage and carcinogenesis.

2024-08-15 | GSE241061 | GEO

RNA-Sequencing of ST2+ Treg cells in response to IL-33 stimulation

Project description:The effects of IL-33 on ST2+ Treg cells were not studied thouroughly. We FACS-sorted in vitro expanded ST2+ Treg cells from C57BL/6 Foxp3-IRES-mRFP (B6 FIR) mice. We next used RNA-seq techonology to define how recombinant IL-33 (rIL-33) may impact mouse Treg by to assessing the transcriptome of IL-33-stimulated ST2+ Treg cells compared to that of untreated ST2+ Treg cells. Our data revealed that ST2+ Treg stimulated with rIL-33 for 6 hours exhibited increased expression of Il10 and Il13 compared to unstimulated ST2+ Treg cells.

2019-05-17 | GSE123922 | GEO

Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

Project description:Bcl6 play a key role in CD4+ T cell development including follicular regulatory T cells. However, the role of Bcl6 in Treg cells in context of allergic inflammation was not fully understood. In this study, we describe the role of Bcl6 in development and function of ST2+Treg cells by analyzing ST2+Treg cell RNA seq.

2020-04-01 | GSE136556 | GEO

RNA-Sequencing of ST2+ Treg cells in response to IL-33 stimulation

Project description:RNA-Sequencing of ST2+ Treg cells in response to IL-33 stimulation

| PRJNA510330 | ENA

Differential roles of TSLP and IL-33 in regulation of Treg cells in progression of colorectal cancer

Project description:Recruitment of regulatory T cells (Tregs) to tumors is a hallmark of cancer progression. However, the role of epithelial cell-derived cytokines in regulation of Treg cells in colorectal cancers is not fully understood. We found a subset of Tregs co-expressing the receptors for thymic stromal lymphopoietin (TSLP) and IL-33 (TSLPR+ST2+ Tregs) was increased in colorectal tumors in humans and mice. This Treg subset expressed high levels of CTLA-4 and PD-1, and TSLPR signaling regulated the expression of CTLA-4 and number of TSLPR+ST2+ Tregs. Treg-specfic deletion of TSLPR resulted in a reduction in tumor number and size, with concomitant increase of Th1 cells in tumors. Similarly, blockade of TSLP effectively inhibited progression of colorectal tumors. On the other hand, TSLPR-ST2+ Tregs highly express Tgfb1 and Pdcd,1 which have been shown to suppress CD8+ T cell immune responses. Collectively, TSLP and IL-33 differentially regulate subsets of Tregs in the progression of colorectal tumor. These data suggest that TSLPR+ST2+ Treg cells are potentially a biomarker, and a therapeutic target for CRC.

2021-12-22 | GSE173124 | GEO

Transcriptional profiling of mouse ST2+ and ST2- Tregs across tissues

Project description:Foxp3+ regulatory T cells (Tregs) are critical mediators of peripheral tolerance and immune homeostasis. Tregs that express the IL-33 receptor ST2 are enriched in peripheral nonlymphoid tissues and can exert a variety of tissue-specific functions from metabolic regulation within adipose tissue to skeletal muscle repair. However, the relationship between ST2+ and ST2- Tregs within and across different tissues remains unclear. To compare murine ST2- and ST2+ Tregs within and across tissues, we performed RNA sequencing (RNAseq) of ST2-CD44hi and ST2+CD44hi Tregs from blood, spleen, lungs, visceral adipose tissue (VAT), colon, and skin. RNAseq was also performed on ST2- CD44lo CD62L+ Tregs from the spleen and lungs. We found that the tissue microenvironment was the major factor shaping the transcriptome of Tregs across tissues. Across the tissues studied, Treg transcriptomes displayed an ordered hierarchy that may represent graded levels of activation or differentiation across tissues. We also identified a core signature that distinguished ST2+ Tregs from ST2- Tregs across tissues and a large number of differentially expressed genes between ST2- and ST2+ Tregs within individual tissues that could support the tissue-specific adaptation and function of ST2+ Tregs. In summary, our work highlights the unique, tissue-specific phenotype of ST2+ Tregs and reveals a core ST2+ Treg transcriptional signature shared across tissues.

2022-07-24 | GSE182322 | GEO

ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

Project description:The role of IL-33 and its receptor ST2 in kidney injury is not well understood. This study demonstrates the importance of ST2 expression on the T-regulatory cells (Tregs) for the resolution of renal injury by suppressing inflammation and fibrosis. Treg-specific deletion of ST2, detrimentally impacted late outcomes of renal injury worsening the impairment of kidney function, inflammation, and fibrosis.

2024-08-27 | GSE272380 | GEO

Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

Project description:Bcl6 restrains ST2+ Treg cell development through negative regulation of Blimp1 in the context of allergic inflammation

| PRJNA562685 | ENA

IL-33 and ST2 license beige and brown adipocytes for uncoupled respiration

Project description:For placental mammals, the transition from the in utero maternal environment to postnatal life requires the activation of thermogenesis to maintain their core temperature. This is primarily accomplished by induction of uncoupling protein 1 (UCP1) in brown and beige adipocytes, the principal sites for uncoupled respiration. Despite its importance, how placental mammals license their thermogenic adipocytes to participate in postnatal uncoupled respiration is not known. Here, we provide evidence that the 'alarmin' IL-33, a nuclear cytokine that activates type 2 immune responses, licenses brown and beige adipocytes for uncoupled respiration. We find that, in absence of IL-33 or ST2, beige and brown adipocytes develop normally but fail to express an appropriately spliced form of Ucp1 mRNA, resulting in absence of UCP1 protein, and impairment in uncoupled respiration and thermoregulation. Together, these data suggest that IL-33 and ST2 function as a developmental switch to license thermogenesis during the perinatal period.

2017-06-10 | GSE83229 | GEO

Pairwise comparison of ST2+ and ST2- FOXP3+ T cells derived from mouse intestinal tumors

Project description:Colorectal cancer (CRC) was induced in Foxp3/eGFP reporter mice by the azoxymethane/dextran sulphate sodium salt (AOM/DSS) protocol. Mice were injected i.p. with the procarcinogen AOM (12.5 mg/kg of body weight). After 1 week, mice received drinking water supplemented with 2.5% DSS for 5 to 7 days, followed by 2 weeks of regular water. The DSS administration was repeated twice with 2% DSS. Mice were sacrificed at week 11 and lamina propia lymphocytes (LPLs) from the colon were isolated. CD4+FOXP3+ (eGFP+) ST2+ or ST2- Tregs were separated from colonic LPLs of CRC induced mice using a FACSAria II cell sorter. Microarray analysis was performed to analyze if ST2+ FOXP3+ Tregs from the colon of CRC mice present a distinct transcription pattern compared to ST2- FOXP3+ Tregs. By this, the role of ST2 for Treg function during intestinal tumorigenesis should be characterized.

2019-05-31 | E-MTAB-6842 | biostudies-arrayexpress

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