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

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

PROVIDER: PRJNA1287359 | ENA |

REPOSITORIES: ENA

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

| PRJNA902012 | 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.

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

2025-07-09 | GSE301699 | GEO

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Project description:IL-12 protects from psoriasiform skin inflammation

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Foxp3+ regulatory T cells control psoriasiform skin inflammation by restraining a type 1 interferon driven CD8+ T cell response

Project description:Determine how regulatory T-cells restrain the cellular/transcriptional response to Imiquimod treatment in the skin (ears).

2018-06-24 | E-MTAB-6873 | biostudies-arrayexpress

Inflammation and tumor susceptibility in skin cancer

Project description:This SuperSeries is composed of the following subset Series: GSE12248: Genetic architecture of murine skin inflammation and tumor susceptibility GSE21247: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (carcinomas) GSE21263: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas) GSE26273: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (aCGH) Refer to individual Series

2010-12-22 | E-GEOD-21264 | biostudies-arrayexpress

DDX5-sIL-36R in keratinocytes controls skin inflammation

Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.

2020-09-09 | PXD021379 |

Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

Project description:Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

| PRJNA857740 | ENA