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

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

PROVIDER: PRJNA702167 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13724286.fastq.gz	Fastqsanger.gz
	SRR13724287.fastq.gz	Fastqsanger.gz
	SRR13724288.fastq.gz	Fastqsanger.gz
	SRR13724289.fastq.gz	Fastqsanger.gz
	SRR13724290.fastq.gz	Fastqsanger.gz

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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 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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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.

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

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

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

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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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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.

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