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Next Generation Sequencing Facilitates Quantitative Analysis of the effects of compound 5D on ILC2 transcriptome

ABSTRACT: Blocking Orai channels inhibits ILC2 effector function

ORGANISM(S): Mus musculus

PROVIDER: GSE221009 | GEO | 2023/08/10

REPOSITORIES: GEO

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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 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 ICAM-1 on lung ILC2 Transcriptome

Project description:ICAM-1 modulates cytokine expression in ILC2s. While it downregulates the expression of ILC2 key cytokines il5, il13 and il9, it upregulates that of il10.

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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.

2020-02-27 | GSE139573 | GEO

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.

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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 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

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

Expression data of ILC2 cells from Ets1-deleted and littermate control mice

Project description:The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2 ILC2 cells isolated from ETS1-deleted or litter mate control mice were cultured on OP9-DL1 with IL-7 and IL-33. Subsequently, RNA from ICOS+ cells was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate ETS1-dependent genes in developing ILC2 cells.

2016-04-01 | E-GEOD-79742 | biostudies-arrayexpress

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

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