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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE301699 | GEO | 2025/07/09

REPOSITORIES: GEO

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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.

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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.

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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]

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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]

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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.

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