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Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from peripheral blood of severe asthma patients I

ABSTRACT: Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from peripheral blood of severe asthma patients I

PROVIDER: PRJNA882847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21661008_1.fastq.gz	Fastqsanger.gz
	SRR21661008_2.fastq.gz	Fastqsanger.gz
	SRR21661009.fastq.gz	Fastqsanger.gz
	SRR21661009_1.fastq.gz	Fastqsanger.gz
	SRR21661009_2.fastq.gz	Fastqsanger.gz

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Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from peripheral blood of severe asthma patients I

Project description:To investigate the gene expression underlying the intercellular diversity in type 2 cytokine secretion activity of ILC2, we performed time-series measurements of type 2 cytokine secretion activity of ILC2 from the peripheral blood of severe asthma patients after IL-33 stimulation . Single cells were collected separately before stimulation and secretion-negative or -positive cells after stimulation, and performed RNA-seq on each cell for gene expression profiling analysis.

2023-09-13 | GSE213810 | GEO

Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from human peripheral blood

Project description:To investigate the gene expression underlying the intercellular diversity in type 2 cytokine secretion activity of ILC2, we performed time-series measurements of type 2 cytokine secretion activity of ILC2 from human peripheral blood after IL-2/IL-33/TSLP stimulation . Single cells were collected separately before stimulation, in transition state or activated cells after stimulation, and performed RNA-seq on each cell for gene expression profiling analysis.

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Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from human peripheral blood

Project description:Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from human peripheral blood

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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.

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H3K27ac ChIP-seq for lung ILC2 and CD4 T cells in HDM induced asthma

Project description:Lung ILC2 and Th2 cells exhibited similar chromatin activation. However, small fraction of super-enhancers showed ILC2-specific, or T cell specific activation.

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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.

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Epigenome analysis reveals novel aspects of ILC2 activation and supports a pathogenic role in asthma

Project description:Recent studies have shown that group 2 innate lymphoid cells (ILC2s) can drive eosinophilic airway inflammation in mouse models of asthma. Moreover, elevated ILC2 counts and/or activity have been reported in asthmatics, together suggesting that ILC2s play an important role in asthma pathophysiology. However, many aspects of ILC2 biology are not fully understood, including the mechanisms underlying ILC2 activation, the tissue-specific functions of ILC2s during inflammation (e.g. lung versus draining lymph node) and what drives ILC2 plasticity. Importantly, it is unknown whether human (epi)genetic variation associated with asthma susceptibility and persistence can be coupled to ILC2s. We address these questions in our manuscript by studying the epigenome of murine ILC2s obtained from Gata3-reporter mice with eosinophilic airway inflammation as well as human ILC2s obtained from peripheral blood and activated in vitro.

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Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - SLC7A5 and SLC7A8 KO

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ATAC-seq of bone marrow ILC2 lineages and Lung ILC2 steady state

Project description:ATAC-seq were performed for bone marrow ILC2 lineages and lung ILC2 of C57BL/6 mice and G3SEKO mice.

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