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MARCH1 controls an exhaustion-like program of effector CD4+ T cells promoting allergic airway inflammation

ABSTRACT: MARCH1 controls an exhaustion-like program of effector CD4+ T cells promoting allergic airway inflammation

PROVIDER: PRJNA870581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21114648_1.fastq.gz	Fastqsanger.gz
	SRR21114648_2.fastq.gz	Fastqsanger.gz
	SRR21114649_1.fastq.gz	Fastqsanger.gz
	SRR21114649_2.fastq.gz	Fastqsanger.gz
	SRR21114650_1.fastq.gz	Fastqsanger.gz

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MARCH1 controls an exhaustion-like program of effector CD4+ T cells promoting allergic airway inflammation

Project description:Persistent antigenic signalling leads to T cell exhaustion, a dysfunctional state arising in many chronic infections and cancers. Little is known concerning mechanisms limiting exhaustion in immune stimulatory diseases such as asthma. We report that membrane-associated RING-CH1 (MARCH1), the ubiquitin ligase that mediates surface turnover of MHCII and CD86 in professional APCs, plays an essential role in restraining exhaustion of effector CD4+ T cells in a mouse model of asthma. Mice lacking MARCH1 or the ubiquitin acceptor sites of MHCII and CD86 exhibited increased MHCII and CD86 surface expression on lung APCs, and this increase promoted enhanced expression of immune inhibitory receptors by effector CD4+ T cells and inhibited their proliferation. Remarkably, ablation of MARCH1 in mice with established asthma reduced airway infiltration of eosinophils and Th2 cells. Thus, MARCH1 controls exhaustion of effector CD4+ T cells during allergic airway inflammation and may serve as a therapeutic target for asthma.

2022-08-24 | GSE211511 | GEO

Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. Therefore, there should be mechanisms to maintain the capacity of ILC2s to produce TH2 cytokines under chronic inflammatory conditions. Here, we report that Runx proteins are essential to prevent exaggerated activation of ILC2, in part by antagonizing GATA-3 function at steady state. However, during allergic inflammation, the absence of Runx in ILC2s impaired their ability to proliferate and produce effector TH2 cytokines and chemokines, but instead induced expression of T cell exhaustion markers including IL-10 and TIGIT. These exhausted ILC2s were unabale to induce type 2 immune responses against repeated allergen inhalation. Thus, Runx proteins protect ILC2s from exhaustion during continuous allergic inflammation.

2019-01-07 | GSE111871 | GEO

Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

Project description:Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

| PRJNA438449 | ENA

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

Notch signaling licenses allergic airway inflammation by promoting lymph node egress of Th2 cells

Project description:Transcriptome analyses of wildtype and Notch-deficient Th2 cells from mouse models of allergic airway inflammation.

2020-06-08 | GSE125358 | GEO

Transcriptome differences in HCC infiltrated CD8+ T cells in effector and exhaustion state

Project description:CD8+ T cells isolated from HCC tissue were divided into three groups: PD1-TIM3- CD8+ TILs, exhibiting full effector function; PD1-intTIM3+ CD8+ TILs, exhibiting partial exhaustion; and PD1-hiTIM3+ CD8+ TILs, exhibiting severe exhaustion, as reflected by the differences in their ability to produce effector cytokines respectively. Transcriptome sequence analysis was performed to investigate the gene expression profile was performed.

2019-12-31 | E-MTAB-7278 | biostudies-arrayexpress

Eosinophils promote effector functions of lung ILC2s in allergic airway inflammation in mice

Project description:Eosinophils promote effector functions of lung ILC2s in allergic airway inflammation in mice

| PRJNA909795 | ENA

Expression and MeDIP microarray data from IL13-induced allergic airway inflammation of mice lungs

Project description:This SuperSeries is composed of the following subset Series: GSE35979: Gene expression data from IL13-induced allergic airway inflammation of mice lungs GSE35980: MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs GSE37079: Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs Refer to individual Series

2012-04-06 | E-GEOD-37085 | biostudies-arrayexpress

Notch signaling licenses allergic airway inflammation by promoting lymph node egress of Th2 cells

Project description:Notch signaling licenses allergic airway inflammation by promoting lymph node egress of Th2 cells

| PRJNA515916 | ENA

Allergic Airway Disease is Dependent on Methylene-Tetrahydrofolate Reductase (expression)

Project description:RATIONALE: The development and progression of asthma are strongly influenced by environmental exposures. We have demonstrated that mice exposed to a diet enriched with methyl donors during vulnerable periods of fetal development can enhance the heritable risk of allergic airway disease through epigenetic changes. OBJECTIVES: Since there is conflicting evidence on the role of folate in modifying allergic airway disease risk, we hypothesized that blocking folate metabolism through the loss of methylene-tetrahydrofolate reductase (MTHFR) activity would reduce the allergic airway disease phenotype. METHODS: Using a house dust mite (HDM) induced model of allergic airway disease, we tested the effect of MTHFR on disease severity. MEASUREMENTS AND MAIN RESULTS: Loss of MTHFR alters single carbon metabolite levels in the lung and serum including elevated homocysteine and cystathionine and reduced methionine. HDM-treated C57BL/6MTHFR-/- mice demonstrate significantly less airway hyerreactivity (AHR) compared to HDM-treated C57BL/6 mice. Furthermore, HDM-treated C57BL/6MTHFR-/- mice compared to HDM-treated C57BL/6 mice have reduced whole lung lavage (WLL) cellularity, eosinophilia, and IL-4/IL-5 cytokine concentrations. The effect of MTHFR loss on HDM-induced allergic airway disease was reversed by betaine supplementation. 737 genes are differentially expressed and 146 regions are differentially methylated in lung tissue from HDM-treated C57BL/6MTHFR-/- mice and HDM-treated C57BL/6 mice. Additionally, analysis of methylation/expression relationships identified 503 significant correlations. CONCLUSION: Collectively, these findings indicate that single carbon metabolism warrants further investigation as a disease modifier in allergic airway disease.

2018-01-31 | GSE71822 | GEO

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