ArticleFrontiers in immunology2024
NLRP3 deficiency aggravated DNFB-induced chronic itch by enhancing type 2 immunity IL-4/TSLP-TRPA1 axis in mice.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- The neuro-immune insights of itch: peripheral mechanisms and central glial contributions.Cellular & molecular biology letters · 2026Review
- Exploring the Mechanism of Qinzhuliangxue Mixture for Treating Skin Lesions in Atopic Dermatitis: Insights from Network Pharmacology and Experimental Validation.Journal of inflammation research · 2025Article
- Silymarin Exerts Potent Antipruritic Effects Against Chloroquine-Induced Scratching in Mice by Modulating the NO/NF-κB/TRPA1 Pathway.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
8 authors.
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Abstract
Background: The nod-like receptor family pyrin domain-containing 3 (NLRP3) has been implicated in various skin diseases. However, its role in mediating 2, 4-dinitrofluorobenzene (DNFB)-induced chronic itch remains unclear. Methods: Widetype ( Results: This study revealed that the NLRP3 inflammasome was activated in the skin of DNFB-induced chronic itch mice. Surprisingly, the absence of Nlrp3 exacerbated itch behavior. In Discussion: These findings suggested that the absence of Nlrp3 aggravated DNFB-induced chronic itch by exacerbating type 2 immunity in the skin and enhancing the IL-4/TSLP-TRPA1 axis, potentially driven by reduced IL-18 levels.
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Registered trials
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