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

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

PROVIDER: PRJNA744174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15050715_1.fastq.gz	Fastqsanger.gz
	SRR15050715_2.fastq.gz	Fastqsanger.gz
	SRR15050716_1.fastq.gz	Fastqsanger.gz
	SRR15050716_2.fastq.gz	Fastqsanger.gz
	SRR15050717_1.fastq.gz	Fastqsanger.gz

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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 ILC2s]

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 | GSE179551 | GEO

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

2021-07-07 | GSE179546 | GEO

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

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

| PRJNA744187 | 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

Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents

Project description:Thalamic inflammation mediates enhanced seizure risk and altered cognition-related cortical states through astrocytic GAT-3 in mice.

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Rickettsia amblyommatis str. GAT-30V

Project description:Rickettsia amblyommatis str. GAT-30V Genome sequencing

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