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Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [bulk RNA-seq]

ABSTRACT: Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [bulk RNA-seq]

PROVIDER: PRJNA633592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11808617.fastq.gz	Fastqsanger.gz
	SRR11808618.fastq.gz	Fastqsanger.gz
	SRR11808619.fastq.gz	Fastqsanger.gz
	SRR11808620.fastq.gz	Fastqsanger.gz

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Similar Datasets

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition

Project description:Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition

| PRJNA633589 | ENA

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [scRNA-seq]

Project description:Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [scRNA-seq]

| PRJNA633593 | ENA

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [RNA-seq]

Project description:Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [RNA-seq]

| PRJNA640826 | ENA

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [scRNA-seq]

Project description:Type 2 cytokine responses promote parasitic immunity and initiate tissue repair but, can also result in immunopathologies when not properly restricted. Basophilia is recognized as a common feature of type 2 inflammation, however, the roles basophils play in regulating these responses remain unknown. Here, we demonstrate that helminth-induced ILC2 responses are exaggerated in the absence of basophils, resulting in increased inflammation and diminished lung function. Additionally, we show that ILC2s from basophil-depleted mice express reduced levels of the receptor for the neuropeptide, neuromedin B (NMB). Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB receptor (NMBR) expression on ILC2s. These studies suggest that basophils prime ILC2s to respond to neuron-derived signals necessary to maintain tissue integrity. Further, these data provide mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type 2 inflammation.

2020-07-20 | GSE150792 | GEO

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [RNA-seq]

2020-07-20 | GSE152913 | GEO

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition [bulk RNA-seq]

2020-07-20 | GSE150791 | GEO

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition.

Project description:Type 2 cytokine responses promote parasitic immunity and initiate tissue repair; however, they can also result in immunopathologies when not properly restricted. Although basophilia is recognized as a common feature of type 2 inflammation, the roles basophils play in regulating these responses are unknown. Here, we demonstrate that helminth-induced group 2 innate lymphoid cell (ILC2) responses are exaggerated in the absence of basophils, resulting in increased inflammation and diminished lung function. Additionally, we show that ILC2s from basophil-depleted mice express reduced amounts of the receptor for the neuropeptide neuromedin B (NMB). Critically, NMB stimulation inhibited ILC2 responses from control but not basophil-depleted mice, and basophils were sufficient to directly enhance NMB receptor expression on ILC2s. These studies suggest that basophils prime ILC2s to respond to neuron-derived signals necessary to maintain tissue integrity. Further, these data provide mechanistic insight into the functions of basophils and identify NMB as a potent inhibitor of type 2 inflammation.

| S-EPMC9357342 | biostudies-literature

Basophils prime group 2 innate lymphoid cells for neuropeptide-mediated inhibition

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

2020-07-20 | GSE150793 | GEO

The neuropeptide Neuromedin U stimulates innate lymphoid cells and promotes type 2 inflammation

Project description:The neuropeptide Neuromedin U stimulates innate lymphoid cells and promotes type 2 inflammation

| PRJNA395014 | ENA

The neuropeptide Neuromedin U stimulates innate lymphoid cells and promotes type 2 inflammation [NMU]

Project description:The type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 play critical roles in stimulating innate and adaptive immune responses required for resistance to helminth infection and promotion of allergic inflammation, metabolic homeostasis and tissue repair. Group 2 innate lymphoid cells (ILC2s) are a potent source of type 2 cytokines and while significant advances have been made in understanding the cytokine milieu that promotes ILC2 responses, there are fundamental gaps in knowledge regarding how ILC2 responses are regulated by other stimuli. In this report, we demonstrate that ILC2s in the gastrointestinal tract co-localize with cholinergic neurons that express the neuropeptide neuromedin U (NMU). In contrast to other hematopoietic cells, ILC2s selectively express the NMU receptor 1 (NMUR1). In vitro stimulation of ILC2s with NMU induced rapid cell activation, proliferation and secretion of type 2 cytokines IL-5, IL-9 and IL-13 that was dependent on cell-intrinsic expression of NMUR1 and Gaq protein. In vivo administration of NMU triggered potent type 2 cytokine responses characterized by ILC2 activation, proliferation and eosinophil recruitment that was associated with accelerated expulsion of the gastrointestinal nematode Nippostrongylus brasiliensis or induction of lung inflammation. Conversely, worm burden was higher in Nmur1-/- mice compared to control mice. Further, use of gene-deficient mice and adoptive cell transfer experiments revealed that ILC2s were necessary and sufficient to mount NMU-elicited type 2 cytokine responses. Together, these data indicate that the NMU-NMUR1 neuronal signaling circuit provides a selective and previously unrecognized mechanism through which the enteric nervous system and innate immune system integrate to promote rapid type 2 cytokine responses that can induce anti-microbial, inflammatory and tissue-protective type 2 responses at mucosal sites.

2017-08-18 | GSE101624 | GEO

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