Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells

ABSTRACT: DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells

PROVIDER: PRJNA480393 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7503280.fastq.gz	Fastqsanger.gz
	SRR7503281.fastq.gz	Fastqsanger.gz
	SRR7503282.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

DUSP10 constrains innate IL-33-mediated cytokine production in ST2hi memory-type pathogenic Th2 cells

Project description:Memory CD4+ T helper (Th) cells are crucial for acquired immunity and protection from infectious microorganisms, and also drive pathogenesis of chronic inflammatory diseases, such as asthma. ST2hi memory-type Th2 cells have been identified as a pathogenic subpopulation capable of directly inducing eosinophilic airway inflammation. These ST2hi pathogenic Th2 cells produce large amounts of IL-5 upon stimulation via their TCR, but not in response to IL-33. In contrast, IL-33 alone induces cytokine production in ST2+ group 2 innate lymphoid cells (ILC2). We investigated the molecular mechanism that controls the innate function of IL-33-induced cytokine production, and identified a MAPK phosphatase Dusp10, as a key negative regulator of IL-33–induced cytokine production in Th2 cells. We found that Dusp10 is expressed by ST2hi pathogenic Th2 cells but not by ILC2, and Dusp10 expression inhibits IL-33-induced cytokine production by preventing GATA3 activity through inhibition of p38 MAPK phosphorylation. Strikingly, deletion of Dusp10 rendered ST2hi Th2 cells able to directly respond to IL-33 exposure and produce IL-5. Thus, DUSP10 constrains IL-33–induced cytokine production in ST2hi pathogenic Th2 cells by controlling p38-mediated GATA3 function.

2018-09-23 | GSE116842 | GEO

DUSP10 constrains innate IL-33-mediated cytokine production in ST2<sup>hi</sup> memory-type pathogenic Th2 cells.

Project description:ST2hi memory-type Th2 cells are identified as a pathogenic subpopulation in eosinophilic airway inflammation. These ST2hi pathogenic Th2 cells produce large amount of IL-5 upon T cell receptor stimulation, but not in response to IL-33 treatment. By contrast, IL-33 alone induces cytokine production in ST2+ group 2 innate lymphoid cells (ILC2). Here we show that a MAPK phosphatase Dusp10 is a key negative regulator of IL-33-induced cytokine production in Th2 cells. In this regard, Dusp10 is expressed by ST2hi pathogenic Th2 cells but not by ILC2, and Dusp10 expression inhibits IL-33-induced cytokine production. Mechanistically, this inhibition is mediated by DUSP10-mediated dephosphorylation and inactivation of p38 MAPK, resulting in reduced GATA3 activity. The deletion of Dusp10 renders ST2hi Th2 cells capable of producing IL-5 by IL-33 stimulation. Our data thus suggest that DUSP10 restricts IL-33-induced cytokine production in ST2hi pathogenic Th2 cells by controlling p38-GATA3 activity.

| S-EPMC6185962 | biostudies-literature

Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

Project description:This study reveraled that androgen signaling suppresses differentiation and cytokine production of Th2 cells by inducing DUSP-2, explaining, in part, the sex bias of asthma after adolescence.

2022-07-13 | GSE200840 | GEO

Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

Project description:Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

| PRJNA826897 | ENA

TMT Multiplexing-Based Quantitative Analysis of Pathogenic Th2 Proteomes.

Project description:To investigate the regulation of pathogenic Th2 (pTh2) cells and the role of histone deacetylase 1 (HDAC1) in the respective processes, we used a new in vitro protocol for generating pTh2 cells and performed qunatitative mass spectrometry analysis based on TMTpro 16plex multiplexing to analyze proteomes. We profiled classical Th2 and pTh2 cells from wild type (WT) mice and mice with a T cell-specific deletion of HDAC1 (HDAC1-cKO).

2025-02-20 | PXD042975 | Pride

Effect of HDAC1 deficiency on in vitro Th2 and pathogenic Th2 differentiated murine CD4+ T cells

Project description:The differentiation of naïve CD4+ T cells into distinct effector T helper (Th) subsets is controlled by the chromatin state of the cells which in turn is regulated by various epigenetic mechanisms such as reversible lysine acetylation mediated by histone acetyltransferases and histone deacetylases (HDACs). In addition, Th2 cells can aquire pathogenic features, secreting pro-inflammatory factors and high levels of the cytokine IL-5. By using HDAC1 deficient naïve CD4+ T cells and establishing a protocol for differentiation of pathogenic Th2 cells, we could establish a critical role for HDAC1 in regulating the differentiation and pathogenicity of in vitro generated pathogenic Th2 cells

2025-01-23 | GSE235803 | GEO

Transcriptional profiling of TH2 cells identifies pathogenic features associated with asthma

Project description:Allergic asthma and rhinitis are two common chronic allergic diseases that affect the lungs and nose, respectively. Both diseases share clinical and pathological features characteristic of excessive allergen-induced type 2 inflammation, orchestrated by memory CD4+ T cells that produce type 2 cytokines (TH2 cells). However, a large majority of subjects with allergic rhinitis do not develop asthma, suggesting divergence in disease mechanisms. Since TH2 cells play a pathogenic role in both these diseases and are also present in healthy non-allergic subjects, we performed global transcriptional profiling to determine whether there are qualitative differences in TH2 cells from subjects with allergic asthma, rhinitis and healthy controls. TH2 cells from asthmatic subjects expressed higher levels of several genes that promote their survival as well as alter their metabolic pathways to favor persistence at sites of allergic inflammation. In addition, genes that enhanced TH2 polarization and TH2 cytokine production were also upregulated in asthma. Several genes that oppose T cell activation were downregulated in asthma, suggesting enhanced activation potential of TH2 cells from asthmatic subjects. Many novel genes with poorly defined functions were also differentially expressed in asthma. Thus, our transcriptomic analysis of circulating TH2 cells has identified several molecules that are likely to confer pathogenic features to TH2 cells that are either unique or common to both asthma and rhinitis.

2016-06-01 | GSE75011 | GEO

TH2

Project description:Arabidopsis thaliana TH2, Bifunctional TH2 protein, mitochondrial [Source:UniProtKB/Swiss-Prot;Acc:F4KFT7], is differentially expressed in 35 experiment(s);

| AT5G32470 | ExpressionAtlas

TH2

Project description:Arabidopsis thaliana TH2, Bifunctional TH2 protein, mitochondrial [Source:UniProtKB/Swiss-Prot;Acc:F4KFT7], is expressed in 15 baseline experiment(s);

| AT5G32470 | ExpressionAtlas

IL-33-activated calcitonin gene-related peptide-producing memory Th2 cells co-operate with somatosensory neurons to induce conjunctival itch

Project description:Allergic conjunctivitis is a chronic inflammatory disease that is characterized by severe itch in the conjunctiva; but how neuro-immune interactions shape the pathogenesis of severe itch remains unclear. We identified a subset of memory-type pathogenic Th2 cells that preferentially expressed Il1rl1-encoding ST2 and Calca-encoding calcitonin gene-related peptide (CGRP) in the inflammatory conjunctiva using a single-cell analysis. The IL-33-ST2 axis in memory Th2 cells controlled the axonal elongation of the peripheral sensory C-fiber and the induction of severe itch. Pharmacological blockade and genetic deletion of CGRP signaling in vivo attenuated scratching behavior. The analysis of giant papillae from patients with severe allergic conjunctivitis revealed ectopic lymphoid structure formation with the accumulation of IL-33-producing epithelial cells and CGRP-producing pathogenic CD4+ T cells accompanied by peripheral nerve elongation. Thus, the IL-33-ST2-CGRP axis directs severe itch with neuro-reconstruction in the inflammatory conjunctiva and is a potential therapeutic target for severe itch in allergic conjunctivitis.

2022-05-20 | GSE203217 | 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