ArticleThe Journal of allergy and clinical immunology2022
IL-33 signaling in sensory neurons promotes dry skin itch.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.
- Pathogenesis and Therapeutics for Chronic Pruritus of Unknown Origin: A Systematic Review.International journal of dermatology · 2026Pooled it
- The role of IL-33 in depression: a systematic review and meta-analysis.Frontiers in psychiatry · 2023Pooled it
- Neuro-immune interactions in tumors, immune-related disorders, and infections.Signal transduction and targeted therapy · 2026Review
- Integrative Approaches to Atopic Dermatitis: Exploring Biomarkers, Current Therapies, and the Potential Role of Osteopathic Manipulative Medicine.International journal of molecular sciences · 2026Review
- Article
- Shared Mechanistic Pathways in Bullous Pemphigoid, Chronic Spontaneous Urticaria, Prurigo Nodularis, and Chronic Prurigo of Unknown Origin: Implications for Targeted Therapies.American journal of clinical dermatology · 2026Review
- Immunopathogenesis of itch: an integrative framework for chronic pruritus.JID innovations : skin science from molecules to population health · 2026Review
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Mechanisms of pruritus and advances in traditional Chinese medicine therapy (Review).Molecular medicine reports · 2026Review
- Review
- Therapeutic advances in pruritus as a model of personalized medicine.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Review
- From neuroimmune circuits to targeted therapy of chronic pruritus.Pharmacological reviews · 2026Review
- A "controlled assembly" strategy for constructingBioactive materials · 2026Article
- The neuro-immune insights of itch: peripheral mechanisms and central glial contributions.Cellular & molecular biology letters · 2026Review
- Spinal and supraspinal mechanisms of chronic itch: from neuronal circuits to the neuro-immune-microbial axis.Frontiers in medicine · 2026Review
- Neuronal Mechanisms of Psoriatic Itch: Role of IL-17R/ERK/TRPV4 Signaling Pathway.The Journal of investigative dermatology · 2025Article
- Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation.bioRxiv : the preprint server for biology · 2025Article
- IL-31/33 Axis in Atopic Dermatitis.International journal of molecular sciences · 2025Review
- Long-term scratching analysis of mice using machine learning.PNAS nexus · 2025Article
- Targeting Vascular and Inflammatory Crosstalk: Cannabigerol as a Dual-Pathway Modulator in Rosacea.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundChronic pruritus, or itch, is common and debilitating, but the neuroimmune mechanisms that drive chronic itch are only starting to be elucidated. Recent studies demonstrate that the IL-33 receptor (IL-33R) is expressed by sensory neurons. However, whether sensory neuron-restricted activity of IL-33 is necessary for chronic itch remains poorly understood.
objectivesWe sought to determine if IL-33 signaling in sensory neurons is critical for the development of chronic itch in 2 divergent pruritic disease models.
methodsPlasma levels of IL-33 were assessed in patients with atopic dermatitis (AD) and chronic pruritus of unknown origin (CPUO). Mice were generated to conditionally delete IL-33R from sensory neurons. The contribution of neuronal IL-33R signaling to chronic itch development was tested in mouse models that recapitulate key pathologic features of AD and CPUO, respectively.
resultsIL-33 was elevated in both AD and CPUO as well as their respective mouse models. While neuron-restricted IL-33R signaling was dispensable for itch in AD-like disease, it was required for the development of dry skin itch in a mouse model that mirrors key aspects of CPUO pathology.
conclusionsThese data highlight how IL-33 may be a predominant mediator of itch in certain contexts, depending on the tissue microenvironment. Further, this study provides insight into future therapeutic strategies targeting the IL-33 pathway for chronic itch.
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Registered trials
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