Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE182322 | GEO | 2022/07/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Role of ST2 expession in regulatory Tcells on muscle regneration

Project description:We describe the effects of Treg ST2 expression on muscle regeneration. We compare regneration from cryo-injured tibialis anterior muscle from Foxp3-Cre/ST2-flox vs Foxp3-Cre mice 8 days post-injury. These analyses from whole muscle provide insight into the role of muscle Tregs in the context of regeneration. The tibialis anterior muscle from male Foxp3-Cre/ST2 flox or Foxp3-Cre/ST2 WT C57BL/6 mice (2 months old) were cryo-injured using a liquid nitrogen chilled metal probe for 8 seconds. 8 days post-injury whole muscle was harvested and snap frozen in liquid nitrogen. Whole muscle was then homogenized directly in TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

2016-01-10 | E-GEOD-76697 | biostudies-arrayexpress

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

Project description:Transcriptional profiling of mouse ST2+ and ST2- Tregs across tissues

| PRJNA755747 | ENA

The distinct function and control of regulatory T cell subsets during influenza infection

Project description:During influenza infection, Treg cells in the lung acquire at least 3 discernable phenotypes which can be characterized by the expression of the IL-33 receptor ST2, the Th1 associated chemokine receptor CXCR3 or neither receptor. It is known in the Treg field that Treg cell acquire different phenotypes to more specifically target related immune responses. For example, Th1 like CXCR3 expressing Treg cells are thought to traffic to and specifically suppress adaptive type 1 immune responses. We have found that during influenza infection, ST2+ Treg cells specifically target innate immune responses characterized by IL-1 mediated neutrophil and eosinophil recruitment and the activation of IL17 producing gamma delta T cells. In order to determine how ST2+ Treg cell perform their specific immunomodulatory function, we have performed RNAseq transcriptomic analysis to compare gene expression in ST2+ Tregs isolated from day 7 influenza infected lungs with CXCR3+ Treg cells and Treg cells expressing neither marker also from day 7 of influenza infected lungs as well as compared to total Treg cells from the spleen of uninfected mice.

2022-03-31 | GSE173249 | GEO

Role of ST2 expession in regulatory Tcells on muscle regneration

2016-01-10 | GSE76697 | 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

Single-cell expression profiling of visceral adipose tissue and splenic CD4+ T cells from Treg-bmal1WT and Treg-bmal1KO mice at ZT0 and ZT12.

Project description:we reported single-cell gene expression of CD4+ T cells from the visceral adipose tissue of from male Foxp3-Cre.YFP bmal1WT or Foxp3-Cre.YFP bmal1flox/flox mice, and from spleen from bmal1WT mice, at ZT0 or ZT12. We found that VAT Tregs could be subdivided into five subtypes: p1 ST2+, p2 ST2+, Tbet+, IL18r+ and resting clusters. We found diurnal variation within the ST2+ subgroups, where the more activated p1 ST2+ Tregs were more represented at ZT0 in WT VAT Tregs. Such variations were not observed in splenic Tregs. In contrast, bmal1KO VAT Tregs were were enriched in the ST2+ Tregs, and had a constitutively high proportion of the p1 ST2+ subtype at ZT0 and ZT12.

2022-07-28 | GSE206949 | GEO

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

Tumor-Infiltrating Regulatory T Cell Accumulation in the Tumor Microenvironment is Mediated by IL33/ST2 Signaling

Project description:Regulatory T cells (Tregs) are enriched in the tumor microenvironment (TME) and suppress anti-tumor immunity. However, the origin of tumor-infiltrating (TI) Tregs and the molecular mechanism underlying their TME accumulation are poorly understood. Although IL-33 was reported to regulate the expansion and function of Tregs, its direct role on TI Tregs and its contribution to tumor progression remain uncertain. Firstly, we demonstrated TI Tregs were primarily thymus-derived. More importantly, we found using comparative transcriptome analysis that proliferation-related genes were prominently upregulated in TI Tregs compared with TI CD4+Foxp3− conventional T cells or splenic Tregs of same tumor-bearing mice. One of these genes, ST2, an interleukin-33 (IL-33) receptor, was identified as a potential factor driving Treg accumulation in the TME. Indeed, IL-33-directed ST2 signaling induced the preferential proliferation of TI Tregs and enhanced tumor progression, while genetic deletion of ST2 in Tregs limited their TME accumulation and delayed tumor growth. These data demonstrate the IL-33/ST2 axis in Tregs as one of the critical pathways for the preferential accumulation of thymus-derived Tregs in the TME and suggest the axis as a potential therapeutic target for cancer immunotherapy.

2020-08-12 | GSE152022 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data