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

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

PROVIDER: PRJNA744190 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15050914.fastq.gz	Fastqsanger.gz
	SRR15050915.fastq.gz	Fastqsanger.gz
	SRR15050916.fastq.gz	Fastqsanger.gz
	SRR15050917.fastq.gz	Fastqsanger.gz
	SRR15050918.fastq.gz	Fastqsanger.gz

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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 [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

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress

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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Proteome of group 2 innate lymphoid cells (ILC2s) stimulated with IL33 and TL1A

Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.

2024-03-05 | PXD041987 | Pride

Rickettsia amblyommatis str. GAT-30V

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

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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

Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s)

Project description:Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s).

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