ReviewCurrent allergy and asthma reports2026
Cross-Talk between Neurons and Immune Cells in Pruritus: from Mechanisms To Medicines.
Review in Current allergy and asthma reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- The Mast Cell-Substance P Neuroimmune Axis in Allergic Contact Dermatitis and Atopic Dermatitis: Molecular Mechanisms and Pathophysiological Perspectives.Current issues in molecular biology · 2026Review
- Sex- and Gender-Related Differences in Pruritus in Dermatological Diseases: Insights into Inflammatory, Autoimmune, and Connective Tissue Disorders.Life (Basel, Switzerland) · 2026Review
- Arthropod Exposure-Associated Neurogenic Pruritus: A Complex Neuro-Immune Transition Mimicking Refractory Urticaria.Cureus · 2026Article
- Targeting type 2 inflammation in dermatology: mechanisms and clinical implications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewChronic pruritus (CP) is among the most distressing symptoms and has a complex pathophysiology. This review aims to describe the mediators and mechanisms of neuroimmune crosstalk—a term referring the bidirectional interactions between the nervous and immune systems that underly itch pathogenesis and chronicity. RECENT
findingsType 2 cytokines (IL-4, IL-13, IL-31) directly activate pruriceptive neurons, resulting in itch sensation and nerve fiber sensitization via TRPV1/TRPA1, whereas keratinocyte-derived alarmins (TSLP and IL-33) amplify neural activation. Periostin, an emerging downstream mediator, binds integrin αVβ3 on neurons and induces macrophage IL-31 release, representing a link between immune and neural pathways. BNP, another emerging mediator that is co-expressed with IL-31, facilitates itch signaling in the spinal cord and induces keratinocyte production of itch mediators, highlighting its integral role in neuroimmune signaling. CP arises from a complex interplay between the immune system, sensory neurons, and keratinocytes. The success of therapeutic advances targeting cytokines, neuropeptides, and their receptors in recent years have confirmed the importance of understanding these complex underlying networks.
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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.