Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit

ABSTRACT: Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit

PROVIDER: PRJNA744187 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15050914.fastq.gz	Fastqsanger.gz
	SRR15050715_1.fastq.gz	Fastqsanger.gz
	SRR15050715_2.fastq.gz	Fastqsanger.gz
	SRR15050915.fastq.gz	Fastqsanger.gz
	SRR15050716_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 33

Similar Datasets

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT MSCs]

Project description:Signals from sympathetic neurons and immune cells regulate adipocytes contributing to fat tissue biology. Interactions between the nervous and immune systems have recently emerged as major regulators of host defence and inflammation1-4. Nevertheless, whether neuronal and immune cells cooperate in brain-body axes to orchestrate metabolism and obesity remains elusive. Here we report a novel neuro-mesenchyme unit that controls group 2 innate lymphoid cells (ILC2), adipose tissue physiology, metabolism and obesity via a brain-adipose circuit. We found that sympathetic nerve terminals act on neighbouring adipose mesenchymal cells via the beta-2 adrenergic receptor to control the expression of the glial-derived neurotrophic factor (GDNF) and the activity of ILC2 in gonadal fat. Accordingly, ILC2-autonomous manipulation of the GDNF receptor machinery led to altered ILC2 function, energy expenditure, insulin resistance and propensity to obesity. Retrograde tracing, chemical, surgical and chemogenetic manipulations identified a sympathetic aorticorenal circuit that modulates gonadal fat ILC2 and connects to high-order brain areas, including the paraventricular nucleus of the hypothalamus (PVH). Our work decodes a neuro-mesenchymal unit that translates long-range neuronal circuitry cues into adipose-resident ILC2 function, shaping the host metabolism and obesity.

2021-07-07 | GSE179546 | GEO

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT ILC2s]

2021-07-07 | GSE179551 | GEO

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT ILC2s]

Project description:Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT ILC2s]

| PRJNA744190 | ENA

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT MSCs]

Project description:Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit [GAT MSCs]

| PRJNA744174 | ENA

Neuro-mesenchyme units control ILC2 and obesity via a brain-adipose circuit

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-07 | GSE179553 | 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

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 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

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data