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A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [plate scRNA-seq]

ABSTRACT: A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [plate scRNA-seq]

PROVIDER: PRJNA902012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22304400_1.fastq.gz	Fastqsanger.gz
	SRR22304400_2.fastq.gz	Fastqsanger.gz
	SRR22304500_1.fastq.gz	Fastqsanger.gz
	SRR22304500_2.fastq.gz	Fastqsanger.gz
	SRR22304600_1.fastq.gz	Fastqsanger.gz

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A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation.

Project description:A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation.

| PRJNA1287359 | ENA

A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [fixed scRNA-seq]

Project description:A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [fixed scRNA-seq]

| PRJNA1285691 | ENA

A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [plate scRNA-seq]

Project description:The skin, as a principal barrier tissue, integrates diverse signals discerned by sensory neurons and by immune cells to elicit adaptive responses to a wide range of stresses. While nociceptors, sensory neurons that initiate the sensation of pain, can mobilize and amplify the function of innate and adaptive immune effector cells, regulatory T (Treg) cells, a T cell subset expressing the transcription factor Foxp3, suppress systemic and local inflammatory responses. Considering the connectivity between nervous and immune systems for sensing and responding to damaging insults, we questioned whether Treg cells can modulate proinflammatory neuronal activity by acting directly on peripheral neurons. We found that Treg cells localized near axons innervating the skin and that short-term inactivation or ablation of Treg cells increased neuronal activation to noxious stimuli in a manner separable from their immunosuppressive function. Furthermore, a population of skin Treg cells was highly enriched for expression of Penk, the gene encoding the neuropeptide precursor for endogenous opioids enkephalins, which inhibit pain perception by inducing analgesia. Acute depletion of Penk expressing Treg cells, or inducible ablation of Penk in Treg cells increased neuronal activation in response to noxious stimuli and associated inflammation. Our study suggests that a population of Treg cells residing at barrier tissues exhibit a direct neuromodulatory activity opposing exacerbated activation of sensory neurons, at least in part through the production of an endogenous opioids, and by acting as an immune component of the neuro-immune axis, dampen responses to noxious pain stimuli and local inflammation.

2023-11-14 | GSE218063 | GEO

A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation [fixed scRNA-seq]

Project description:The skin integrates diverse signals discerned by sensory neurons and immune cells to elicit adaptive responses to a range of stresses. Considering interactions between nervous and immune systems, we questioned whether regulatory T (Treg ) cells, that suppresses systemic and local inflammation, can modulate activation of peripheral neurons. Acute Treg cell “loss-of-function” increased neuronal activation to noxious stimuli independently from immunosuppressive function. We find that a population of activated skin Treg cells is highly enriched for Penk expression, a precursor for endogenous opioid enkephalins. Punctual selective depletion of Penk-expressing Treg cells, or specific ablation of Penk in Treg cells increases neuronal activation in response to noxious stimuli and associated inflammation. Our study indicates that a population of tissue Treg cells exhibits neuromodulatory activity to restrain local inflammation.

2025-07-09 | GSE301586 | GEO

A population of Regulatory T cells controls nociception through enkephalins to restrain skin inflammation.

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

2025-07-09 | GSE301699 | GEO

C57BL/6 substrain differences in inflammatory and neuropathic nociception and genetic mapping of a major quantitative trait locus underlying acute thermal nociception

Project description:Sensitivity to different pain modalities has a genetic basis that remains largely unknown. The use of closely related inbred mouse strains can facilitate gene mapping of nociceptive behaviors in preclinical pain models. We previously reported enhanced sensitivity to acute thermal nociception in C57BL/6J (B6J) versus C57BL/6N (B6N) substrains. Here, we expanded on pain phenotypes and observed an increase in inflammatory nociceptive behaviors induced by hindpaw formalin injections in B6J versus B6N mice (Charles River Laboratories). No strain differences were observed in mechanical or thermal hypersensitivity or in paw diameter following the Complete Freund s Adjuvant (CFA) model of inflammatory pain, indicating specificity in the inflammatory nociceptive stimulus. In the chronic nerve constriction injury (CCI), a model of neuropathic pain, no strain differences were observed in baseline mechanical threshold or in mechanical hypersensitivity up to one month post-CCI. We replicated the enhanced thermal nociception in B6J mice in the 52.5 C hot plate test relative to B6N mice from The Jackson Laboratory. Using a B6J x B6N-F2 cross (N=164), we mapped a major QTL underlying hot plate sensitivity to chromosome 7 that peaked at 26 Mb (LOD = 3.81, 8.74 Mb-36.50 Mb) that was more pronounced in males. Genes containing expression QTLs (eQTLs) associated with the peak nociceptive marker that have been implicated in pain and inflammation include Ryr1, Cyp2a5, Pou2f2, Clip3, Sirt2, Actn4, and Ltbp4 (FDR < 0.05). Future studies involving positional cloning and gene editing will determine the quantitative trait gene(s) and potential pleiotropy of this locus across other pain modalities. RNA-seq data and genotype information from striatum punches of F2 C57BL/6J (B6J) cross C57BL/NJ (B6NJ) oxycodone-treated mice. Genotypes are given relative to B6J allele, eg 0 = homozygous B6J.

2018-11-26 | GSE119719 | GEO

RORα-expressing T regulatory cells restrain allergic skin inflammation.

Project description:Atopic dermatitis is an allergic inflammatory skin disease characterized by the production of the type 2 cytokines in the skin by type 2 innate lymphoid cells (ILC2s) and T helper 2 (TH2) cells, and tissue eosinophilia. Using two distinct mouse models of atopic dermatitis, we show that expression of retinoid-related orphan receptor α (RORα) in skin-resident T regulatory cells (Tregs) is important for restraining allergic skin inflammation. In both models, targeted deletion of RORα in mouse Tregs led to exaggerated eosinophilia driven by interleukin-5 (IL-5) production by ILC2s and TH2 cells. Expression of RORα in skin-resident Tregs suppressed IL-4 expression and enhanced expression of death receptor 3 (DR3), which is the receptor for tumor necrosis factor (TNF) family cytokine, TNF ligand-related molecule 1 (TL1A), which promotes Treg functions. DR3 is expressed on both ILC2s and skin-resident Tregs Upon deletion of RORα in skin-resident Tregs, we found that Tregs were no longer able to sequester TL1A, resulting in enhanced ILC2 activation. We also documented higher expression of RORα in skin-resident Tregs than in peripheral blood circulating Tregs in humans, suggesting that RORα and the TL1A-DR3 circuit could be therapeutically targeted in atopic dermatitis.

| S-EPMC5912895 | biostudies-literature

Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation [scRNA-seq]

Project description:Eosinophils Restrain Humoral Alloimmunity after Lung Transplantation [scRNA-seq]

| PRJNA925481 | ENA

Inhibition of spinal cord Hsp90 enhances morphine anti-nociception by activating an ERK/RSK pathway

Project description:Morphine and other opioids continue to be commonly utilized as clinical analgesics, despite their numerous adverse side effects, including respiratory depression, addiction, and tolerance. The modulation of µ-opioid receptor (MOR) signaling and subsequent behavioral output is one viable approach to improve opioid therapy. Heat shock protein 90 (Hsp90) is a molecular chaperone protein that has recently been implicated in downstream MOR signaling within the brain in mice. Here we identify a context-dependent impact on MOR signaling in which the inhibition of Hsp90 within the spinal cord promotes morphine induced anti-nociception. We show that intrathecal and not systemic administration of the Hsp90 inhibitors 17-AAG or KU-32 amplifies morphine-induced anti-nociception in both thermal and mechanical pain models. Further, we demonstrate that the inhibition of Hsp90 allows for ERK phosphorylation after opioid treatment. ERK activation was localized within the dorsal horns of the spinal cord, which are heavily populated with primary afferents responsible for nociception. The behavioral effects observed with Hsp90 inhibitors were abolished upon intrathecal U0126 (ERK inhibitor) and cycloheximide (translation inhibitor) treatment, suggesting that downstream ERK phosphorylation and rapid protein translation are responsible for the observed amplification of anti-nociception. Quantitative proteomic analysis identified upregulated RSK with spinal cord Hsp90 inhibition, which we further found was necessary for the observed enhancement of anti-nociception. Taken together, we have uncovered a novel downstream MOR ERK/RSK cascade, localized to the spinal cord and repressed by Hsp90, whose modulation may allow for enhanced efficacy and decreased side effects during opioid therapy.

2020-04-24 | PXD015060 | Pride

Transcription profiling of dicer knock-out nociceptive sensory neurons from mice to investigate the roles of microRNAs in nociception

Project description:We used the Nav1.8-Cre to delete Dicer in mouse nociceptive sensory neurons to investigate the roles of microRNAs in nociception.

2010-01-01 | E-MEXP-1461 | biostudies-arrayexpress

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