Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE173249 | GEO | 2022/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CXCR3+ Treg cells suppress Th1-immune responses through expression of the co-inhibitory receptors CD85k and Lag-3

Project description:CD4+Foxp3+ Treg cells are essential for maintaining self-tolerance and preventing excessive immune responses. In the context of Th1 immune responses, co-expression of the Th1 transcription factor T-bet with Foxp3 is essential for Treg cells to control Th1 responses. T-bet-dependent expression of CXCR3 directs Tregs to the site of inflammation, however, the suppressive mediators enabling effective control of Th1 responses at this site are unknown. In this study, we determined the signature of CXCR3+ Treg cells arising in Th1 settings and defined universal features of Treg cells in this context using multiple Th1-dominated models. Our analysis defined a set of Th1-specific co-inhibitory receptors that are specifically expressed in Treg cells during Th1 immune responses. Among these, we identified the novel co-inhibitory receptor CD85k as a functional mediator of the enhanced suppression of Th1 effector cells by CXCR3+ Treg cells.

2018-06-30 | E-MTAB-6156 | biostudies-arrayexpress

Inflammation-dependent differentiation of two distinct regulatory T cell populations in the visceral adipose tissue shapes systemic metabolism [RNA-seq III]

Project description:Visceral adipose tissue (VAT) is an endocrine organ critical for energy storage and metabolic homeostasis. Its function, at least in part, is controlled by immune cells, including Foxp3+ regulatory T (Treg) cells, which restrain VAT inflammation and glucose intolerance. Here we uncover that the VAT harbours two distinct Treg cell populations, prototypical ST2+ Treg cells, that are enriched in males and depend on the cytokine IL-33 and the transcription factor PPAR and a previously uncharacterized population of VAT Treg cells that express the chemokine receptor CXCR3+, are enriched in females and depend on the transcription factor T-bet. We further show that the transcription factor GATA3 promoted differentiation of ST2+ VAT Treg cells and together with PPAR and IL-33 repressed the differentiation of CXCR3+ Treg cells. CXCR3+ VAT Treg cells developed from naïve Treg cells in a cytokine IFN- dependent manner. Finally, we demonstrate that ST2+ Treg cells promoted glucose tolerance, while CXCR3+ Treg cells limited VAT inflammation in a sex specific manner. This study for the first time establishes how inflammation determines the developmental trajectories of two functionally and molecularly distinct Treg cell types in the VAT.

2024-03-22 | GSE237835 | GEO

Inflammation-dependent differentiation of two distinct regulatory T cell populations in the visceral adipose tissue shapes systemic metabolism [RNA-seq II]

2024-03-22 | GSE235420 | GEO

Inflammation-dependent differentiation of two distinct regulatory T cell populations in the visceral adipose tissue shapes systemic metabolism [RNA-seq I]

2024-01-04 | GSE205427 | GEO

Interferon gamma-induction of TH1-like regulatory T cells controls anti-viral responses

Project description:Regulatory T cells (Tregs) are an immunosuppressive population that are required to maintain peripheral tolerance and prevent tissue damage during immunopathology, via anti-inflammatory cytokines, inhibitor receptors and metabolic disruption. We report that Tregs acquire an effector-like state, yet remain stable and functional, when exposed to IFNγ during chronic infection with lymphocytic choriomeningitis (LCMV) and Influenza A virus (IAV). Mechanistically, Treg-restricted-deletion of the IFNγ receptor 1 (IFNGR1), but not the IL12 receptor, prevented TH1-like polarization (decreased expression of T-bet, CXCR3 and IFNγ) and promoted TH2-like polarization (increased expression of GATA-3, CCR4 and IL4). TH1-like Tregs limited CD8+ T cell effector function, proliferation and memory formation during chronic and acute infection. These findings provide fundamental insights into how Tregs sense inflammatory cues from the environment (IFNγ) during viral infection to provide immune guidance to the effector T cell response, to prevent prolonged immunoinflammatory responses and shape the quality of the memory response.

2023-01-23 | GSE223210 | GEO

Regulatory and effector T cells in Lymphocytic choriomeningitis virus WE infection

Project description:In this study, we determined the signature of CD4+Foxp3- effector T cells and CD4+Foxp3+ Treg cells in naive animals and following LCMV WE infection. In addition, transcriptional signatures were determined in CXCR3+ CD4+Foxp3+ Treg cells arising in Th1 settings following LCMV infection.

2020-03-11 | E-MTAB-8861 | biostudies-arrayexpress

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

Blockade of PF4-induced Th1-Treg polarization enhances anti-tumor immunity (Bulk RNA-Seq)

Project description:The tumor microenvironment (TME) contains various immune-suppressive cells such as T helper 1-polarized regulatory T cells (Th1-Tregs). However, little is known about the mechanism behind the abundant presence of Th1-Tregs in TME. In this work, we demonstrate that selective depletion of arginase I (Arg1)-expressing tumor associated macrophages (Arg1+ TAMs) inhibits tumor growth and concurrently reduces the Th1-Treg ratio in TME. Notably, Arg1+ TAMs secrete platelet factor 4 (PF4) that reinforces interferon-γ (IFN-γ)-induced Treg polarization into Th1-Tregs in a manner dependent on CXCR3 and the IFN-γ receptor. Both genetic PF4 inactivation and PF4 neutralization hinder Th1-Treg accumulation in TME, consequently suppressing tumor growth. Collectively, our study highlights the importance of Arg1+ TAM-produced PF4 for high Th1-Treg levels in TME to suppress anti-tumor immunity, and demonstrates PF4 neutralization as a potential cancer immunotherapeutic strategy.

2024-11-07 | GSE252052 | GEO

Distinct roles for IL-27 and IFN-g in the development of T-bet+ Treg required to limit infection-induced pathology

Project description:IL-27 is a potent antagonist of TH1-mediated inflammation, but the basis for this effect is not fully understood. Recent studies identified a population of T-bet+ CXCR3+ Treg that limit TH1-mediated immune pathology. The studies presented here demonstrate that IL-27-mediated STAT1 activation promotes Treg expression of T-bet and CXCR3. Infection with Toxoplasma gondii induced a similar Treg population that limits T cell responses and this population at mucosal sites is IL-27-dependent. Furthermore, transfer of Treg ameliorated the infection-induced CD4+ T cell-mediated pathology observed in IL-27p28-/- mice. Although IFN-γ promoted a similar population of cells in the periphery, it did not compensate for the absence of IL-27 at mucosal sites and microarray analysis revealed that Treg exposed to either cytokine have distinct transcriptional profiles. These findings suggest that IFN-γ and IL-27 have different roles in Treg biology but define IL-27 as a key cytokine that promotes the development of Treg specialized to control TH1 immunity. Three conditions were analyzed across two timepoints. Inducible regulatory T cells (iTreg) were generated in vitro in the presence of IL-27, IFNg or under 'Neutral' conditions as a control. Samples were collected at 10 hours and 2 days during the culture period. Three biological replicates were used for each condition.

2012-09-07 | E-GEOD-38686 | biostudies-arrayexpress

Transcriptional profile of Foxp3+ regulatory T cells from colon lamina propria and mesenteric lymph node in steady state mice

Project description:The IL-33 receptor ST2 is differentially expressed by colonic lamina propria Treg cells Microarray of sort-purified Foxp3+ Treg cells from colonic lamina propria over mesenteric lymph node

2014-06-03 | E-GEOD-58145 | biostudies-arrayexpress

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