Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dissection of in vivo fasting on pancreatic ILC2 function and migration [scRNA-Seq]

ABSTRACT: Dissection of in vivo fasting on pancreatic ILC2 function and migration [scRNA-Seq]

PROVIDER: PRJNA1144152 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30126900_1.fastq.gz	Fastqsanger.gz
	SRR30126900_2.fastq.gz	Fastqsanger.gz
	SRR30126901_1.fastq.gz	Fastqsanger.gz
	SRR30126901_2.fastq.gz	Fastqsanger.gz
	SRR30126902_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Dissection of in vivo fasting on pancreatic ILC2 function and migration [scRNA-Seq]

Project description:Recent studies showed that ILC2 are important regulators of glucose homeostasis. Yet, to date it is not known if fasting influence function and migration of pancreatic ILC2 to help to maintain glucose homeostasis. In this study we showed that enteric sympathetic-ILC2 units respond to low body energy levels, setting an ILC2 gut-pancreatic migration route, leading to increased pancreatic glucagon and maintenance of glucose homeostasis.

2024-08-05 | GSE273960 | GEO

Dissection of in vivo fasting on pancreatic ILC2 function [RNA-Seq]

Project description:Recent studies showed that ILC2 are important regulators of glucose homeostasis. Yet, to date it is not known if fasting influence function of pancreatic ILC2 to help to maintain glucose homeostasis. In this study we showed that enteric sympathetic-ILC2 units respond to low body energy levels, setting an ILC2 gut-pancreatic migration route, leading to increased pancreatic glucagon and maintenance of glucose homeostasis.

2024-08-05 | GSE273959 | GEO

Dissection of in vivo fasting on pancreatic ILC2 function [RNA-Seq]

Project description:Dissection of in vivo fasting on pancreatic ILC2 function [RNA-Seq]

| PRJNA1144153 | ENA

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

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

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

2022-12-22 | PXD038786 | Pride

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.

2024-05-14 | GSE218142 | GEO

Identification of N6-methyladenosine (m6A) modified RNA in activated ILC2

Project description:Innate lymphoid cells (ILCs) are able to directly respond to alarmin signals and produce an array of effector molecules for immune protection and tissue homeostasis. However, how posttranscriptional machinery in ILCs execute extracellular stimuli towards robust gene expression is yet to understand. Here, we reported a cell type-specific role of N6-methyladenosine (m6A) RNA methylation in ILCs. Inducible deletion of m6A methyltransferase METTL3 had little impact on ILC maintenance in the steady state or cytokine-induced ILC1 or ILC3 activation, but dramatically diminished IL-25-triggered ILC2 response. Specific deletion of Mettl3 in ILC2 significantly attenuated cell expansion, cytokine production, inter-organ migration, and anti-helminth immunity. To investigate the molecular mechanism by which m6A modification regulates ILC2 response, we subjected IL-25-activated iILC2 to a m6A-tagged mRNA immunoprecipitation sequencing (meRIP-seq) to identify the m6A modified mRNA.

2023-06-26 | GSE207292 | GEO

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

Project description:ILC2 cells from mice cultured with or without hypoxia for indicated time period were analysed

2022-05-25 | GSE196811 | GEO