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Next Generation Sequencing Facilitates Quantitative Analysis of the effects of TNFa treatment on sorted mouse lung ILC2 Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of the effects of TNFa treatment on sorted mouse lung ILC2 Transcriptomes

PROVIDER: PRJNA552208 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9624720.fastq.gz	Fastqsanger.gz
	SRR9624715.fastq.gz	Fastqsanger.gz
	SRR9624716.fastq.gz	Fastqsanger.gz
	SRR9624717.fastq.gz	Fastqsanger.gz
	SRR9624718.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of the effects of TNFa treatment on sorted mouse lung ILC2 Transcriptomes

Project description:TNFa induces secretion of ILC2 effector cytokines ex vivo. Increased ILC2 activation leads to the development of airway hyperreactiviy and lung inflammation. Targeting TNFa may therefore represent a novel therapeutic target to treat asthma.

2021-07-01 | GSE133672 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of lack of autophagy on sorted mouse lung ILC2 Transcriptomes

Project description:Atg5, a key gene of the autophagy can affect ILC2 effector functions ex vivo. Increased ILC2 activation leads to the development of airway hyperreactivity and lung inflammation. Targeting Atg5 (autophagy) may therefore represent a novel therapeutic target to treat asthma.

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Next Generation Sequencing Facilitates Quantitative Analysis of the effects of PD-1 deficiency on sorted mouse pulmonary ILC2 Transcriptomes

Project description:Allergic asthma is a leading chronic disease associated with airway hyperreactivity (AHR). Type-2 innate lymphoid cells (ILC2s) are a potent source of T-helper 2 cytokines that promote AHR and lung inflammation. In this study, we evaluated the protective role of PD-1 on the development of AHR by focusing on its capacity to regulate ILC2 activation. We find that PD-1 is highly inducible in pulmonary ILC2s and shapes their transcriptional activity, activation and metabolism. Our findings provide new insights regarding the mechanisms of ILC2 regulation, which could be used in innovative approaches for the treatment of allergic asthma.

2020-07-08 | GSE153909 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of CD200R engagment on sorted mouse pulmonary ILC2 Transcriptomes.

Project description:The prevalence of asthma and airway hyperreactivity (AHR) is increasing at an alarming rate. Group 2 innate lymphoid cells (ILC2s) are copious producers of type 2 cytokines, which leads to AHR and lung inflammation. In this study, we demonstrate murine ILC2s express CD200 receptor (CD200R), and this expression is inducible. We ascertain CD200R engagement inhibits activation, proliferation, and type 2 cytokine production, revealing a potent immunoregulatory role for CD200–CD200R axis on ILC2s. Furthermore, we demonstrate that CD200R engagement inhibits both canonical and non-canonical NF-B signaling pathways in activated ILC2s. Importantly, we herein design both preventative and therapeutic approaches utilizing CD200R engagement on ILC2s, which lead to improved airway resistance, dynamic compliance, and eosinophilia. Finally, our results reveal CD200R is expressed on human ILC2s, and its engagement ameliorates AHR in humanized ILC2 models, further emphasizing the translational applications of our findings for treatment of ILC2-related diseases such as allergic asthma.

2021-02-17 | GSE166889 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of CB2 on lung ILC2 Transcriptomes

Project description:CB2 signaling supports secretion of ILC2 effector cytokines ex vivo. Increased ILC2 activation leads to the development of airway hyperreactiviy and lung inflammation. Targeting CB2 signaling may therefore represent a novel therapeutic target to treat asthma.

2021-11-20 | GSE189156 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of IL-10 production on sorted mouse pulmonary ILC2 Transcriptomes.

Project description:ILC2s are the dominant innate lymphoid cell population in the lungs at steady state and their release of type-2 cytokines is a central driver in responding eosinophil infiltration and increased airway hyperreactivity (AHR). For the first time, our laboratory has identified a unique subset of ILC2s in the lungs that produces and secretes IL-10, an anti-inflammatory cytokine, upon stimulation with IL-4. Overall this study introduces a novel, IL-4-inducible IL-10-producing population of ILC210s in the lung are naturally present in a high Th2 model of murine asthma. This research introduces a novel, cell-based immunotherapeutic potential of ILC210s that can be modulated by the signlaing transcription factors Blimp-1 and cMAF, as well as by glucose availability, opening new avenues for the treatment of ILC2-dependent airway inflammation.

2020-10-05 | GSE158983 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of DR-3 agonist on sorted mouse VAT ILC2 Transcriptomes

Project description:Disturbances in glucose homeostasis and low-grade chronic inflammation culminate into metabolic syndrome that increase the risk for the development of type 2 diabetes mellitus (T2DM). The recently discovered type 2 innate lymphoid cells (ILC2s) are capable of secreting copious amounts of type 2 cytokines to modulate metabolic homeostasis in adipose tissue. In this study, we have established that expression of Death Receptor 3 (DR3), a member of the TNF superfamily, on visceral adipose tissue (VAT)-derived murine and peripheral blood human ILC2s is inducible by IL-33. We demonstrate that DR3 engages the canonical and/or non-canonical NF-B pathways, and thus stimulates naïve and co-stimulates IL-33-activated ILC2s. Importantly, DR3 engagement on ILC2s significantly ameliorates glucose tolerance, protects against insulin-resistance onset and remarkably reverses already established insulin-resistance. Taken together, these results convey the potent role of DR3 as an ILC2 regulator and introduce DR3 agonistic treatment as a novel therapeutic avenue for treating T2DM.

2020-07-22 | GSE154823 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of DTA-1 treatment on sorted mouse adipose tissue ILC2 Transcriptomes

Project description:Metabolic syndrome is characterized by disturbances in glucose homeostasis and the development of low-grade systemic inflammation, which increase the risk to develop type-2 diabetes mellitus (T2DM). Type-2 innate lymphoid cells (ILC2s) are a recently discovered immune population secreting Th2-cytokines. While previous studies show how ILC2s can play a critical role in the regulation of metabolic homeostasis in the adipose tissue, a therapeutic target capable of modulating ILC2 activation has yet to be identified. Here, we show that GITR, a member of the TNF superfamily, is expressed on both murine and human ILC2s. Strikingly, we demonstrate that GITR engagement of activated, but not naïve, ILC2s improves glucose homeostasis, resulting in both protection against insulin-resistance onset and amelioration of established insulin-resistance. Together, these results highlight the critical role of GITR as a novel therapeutic molecule against T2DM and its fundamental role as an immune checkpoint for activated ILC2s.

2019-01-01 | GSE123735 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of CD200R engagment on sorted mouse pulmonary ILC2 Transcriptomes.

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of the effects of CD200R engagment on sorted mouse pulmonary ILC2 Transcriptomes.

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Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted mouse pulmonary ILC2 Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted mouse pulmonary ILC2 Transcriptomes

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