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

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

PROVIDER: PRJNA644524 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12162100.fastq.gz	Fastqsanger.gz
	SRR12162101.fastq.gz	Fastqsanger.gz
	SRR12162102.fastq.gz	Fastqsanger.gz
	SRR12162103.fastq.gz	Fastqsanger.gz
	SRR12162104.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

LKB1 prevents ILC2 exhaustion and lung cancer metastasis

Project description:Group 2 innate lymphoid cells (ILC2s) mediate type 2 immune responses involved in anti-helminth immunity, allergic inflammation, and metabolic homeostasis. Recently, they have emerged as key players in regulating tumor immunity. The tumor suppressor liver kinase B1 (LKB1) inactivating mutations is associated with a variety of human cancers, but the role of LKB1 in ILC2 function and ILC2-mediated tumor immunity remains unknown. Here, we show that LKB1 is required for mature ILC2 survival. Ablation of LKB1 in ILC2s results in impaired proliferation and a marked decrease in type 2 cytokine production upon activation, accompanied with the expression of exhaustion signature genes and reduced cellular metabolism, which promote the development of lung melanoma metastasis. In addition, LKB1 deficiency leads to a marked increase of programmed cell death protein-1 (PD-1) expression in ILC2s through activation of nuclear factor of activated T cells (NFAT) pathway. Blockade of PD-1 can restore type 2 cytokine production in LKB1-deficient ILC2 and reverse its exhaustion state, leading to enhanced antitumor immune responses in vivo. Together, our results reveal that LKB1 retrains ILC2 exhaustion state to maintain immune homeostasis and their antitumor immunity.

2024-05-21 | GSE209588 | GEO

Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - WT ILC2

Project description:Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens – including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals, but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 were found to be uniquely pre-primed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine producing capacity of ILC2. Moreover, amino acid determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.

2022-12-22 | PXD038792 | Pride

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.

2020-02-27 | GSE139573 | GEO

Hypoxia Induces Lung Inflammation and Immunity by ILC2 through Stimulating Adrenomedullin from Epithelial Cells

Project description:Hypoxia contributes to airway inflammation and remodeling in several lung diseases; however, exactly how hypoxic pulmonary epithelium regulates allergic inflammation remains to be fully characterized. Here we report that conditional deletion of the E3 ubiquitin ligase VHL in lung epithelial cells resulted in exacerbated type 2 responses accompanied by selective increase of group 2 innate lymphoid cells (ILC2s) at steady state and following inflammation or helminth infection. Ablation of expression of the hypoxia-inducible factor 2 (HIF2a significantly reversed VHL-mediated ILC2 activation. VHL deficiency in lung epithelial cells caused the increased expression of the peptide hormone adrenomedullin (ADM), and our data suggest HIF2a controls Adm expression. ADM directly promoted ILC2 activation both in vitro and in vivo. Our findings indicate that the hypoxic response mediated by the VHL-HIF2a axis is critical for control of pulmonary type 2 responses by increasing ADM expression in lung epithelia causing ILC2 activation.

2022-05-04 | GSE197007 | 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 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.

| PRJNA702167 | ENA

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

| PRJNA720965 | ENA

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