ArticleThe Journal of allergy and clinical immunology2024
IL-33 potentiates histaminergic itch.
Article in The Journal of allergy and clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Review
- A neuroimmune axis linking S100A8/9 to itch sensitization in both bullous pemphigoid and atopic dermatitis.JID innovations : skin science from molecules to population health · 2026Article
- Neuro-immune Crosstalk in Atopic Dermatitis: A Multiaxial Regulatory Network and Novel Therapeutic Perspectives.Clinical reviews in allergy & immunology · 2026Review
- Transient Receptor Potential (TRP) Channels as Fundamental Regulators of Fibrosis and Pruritus-A New Therapeutic Target for Pathological Scar Management.International journal of molecular sciences · 2026Review
- Neuro-immune interactions in urticaria:a pruritus-centric dissection.Frontiers in immunology · 2026Review
- Cytokine imbalance and immune network endotypes underlying heterogeneous response to omalizumab in chronic spontaneous urticaria.Frontiers in immunology · 2026Article
- T Cell/Mast Cell Crosstalk in the Skin of Patients Suffering From Immune-Mediated Diseases, Focusing on Chronic Spontaneous Urticaria.Clinical and translational allergy · 2026Review
- Genetic Variation A118G in the OPRM1 Gene Underlies the Dimorphic Response to Epidural Opioid-Induced Itch.Neuroscience bulletin · 2025Article
- Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation.bioRxiv : the preprint server for biology · 2025Article
- The spatial and single-cell landscape of skin: Charting the multiscale regulation of skin immune function.Seminars in immunology · 2025Review
- Exosomes: A Promising Cell-Free Therapeutic Tool for Treating Cutaneous Nerve Injuries and Promoting Wound Healing.International journal of molecular sciences · 2025Review
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- Depletion of eosinophils during sensitization but not challenge phase in mice blocks the development of food allergy early in life.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Beyond the itch: the complex interplay of immune, neurological, and psychological factors in chronic urticaria.Journal of neuroinflammation · 2025Review
- Neurogenic inflammation and itch in barrier tissues.Seminars in immunology · 2025Review
- Update on type 2 immunity.The Journal of allergy and clinical immunology · 2025Review
- Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation.Science (New York, N.Y.) · 2025Article
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- Alarmins in Chronic Spontaneous Urticaria: Immunological Insights and Therapeutic Perspectives.Biomedicines · 2024Review
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundItch is a common symptom that can greatly diminish quality of life. Histamine is a potent endogenous pruritogen, and while antihistamines are often the first-line treatment for itch, in conditions like chronic spontaneous urticaria (CSU), many patients remain symptomatic while receiving maximal doses. Mechanisms that drive resistance to antihistamines are poorly defined.
objectivesSignaling of the alarmin cytokine IL-33 in sensory neurons is postulated to drive chronic itch by inducing neuronal sensitization to pruritogens. Thus, we sought to determine if IL-33 can augment histamine-induced (histaminergic) itch.
methodsItch behavior was assessed in response to histamine after IL-33 or saline administration. Various stimuli and conditional and global knockout mice were utilized to dissect cellular mechanisms. Multiple existing transcriptomic data sets were evaluated, including single-cell RNA sequencing of human and mouse skin, microarrays of isolated mouse mast cells at steady state and after stimulation with IL-33, and microarrays of skin biopsy samples from subjects with CSU and healthy controls.
resultsIL-33 amplifies histaminergic itch independent of IL-33 signaling in sensory neurons. Mast cells are the top expressors of the IL-33 receptor in both human and mouse skin. When stimulated by IL-33, mouse mast cells significantly increase IL-13 levels. Enhancement of histaminergic itch by IL-33 relies on a mast cell- and IL-13-dependent mechanism. IL-33 receptor expression is increased in lesional skin of subjects with CSU compared to healthy controls.
conclusionsOur findings suggest that IL-33 signaling may be a key driver of histaminergic itch in mast cell-associated pruritic conditions such as CSU.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.