ArticleAllergy2026
Sensitizer-Induced Basophils Accelerate Skin Re-Epithelialization via IL-4/IL-13-Mediated Macrophage Polarization.
Article in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Immunometabolic control of macrophage plasticity in wound healing: mechanistic insights and therapeutic opportunities.Frontiers in immunology · 2026Review
- MDI1228, a topical pan-JAK inhibitor, disrupts dermal fibroblast-T cell chemokine crosstalk to resolve allergic contact and atopic dermatitis.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundAtopic dermatitis (AD) patients exhibit a paradox of impaired skin barrier with intense itching, yet often demonstrate rapid re-epithelialization after scratching. While basophils are key effector cells in allergic inflammation, their role in the subsequent tissue repair remains unexplored.
objectiveWe investigated whether basophils, recruited during sensitized skin responses, contribute to wound healing.
methodsUsing single-cell RNA sequencing, flow cytometry, and immunofluorescence, we mapped basophil infiltration and activation in sensitizer (oxazolone)-induced skin injury models. We employed genetic (Mcpt8
resultsWe identified a significant enrichment of basophils in wounded skin, peaking at day 3-6 post-injury. Sensitizer-challenge enhanced basophil recruitment and accelerated wound closure, angiogenesis, and re-epithelialization. Depletion of basophils severely impaired these repair processes. Mechanistically, basophils were the predominant source of IL-4 and IL-13 in the early wound microenvironment. These cytokines were essential for driving macrophage polarization toward a pro-repair M2 phenotype. Loss of IL4/IL13 specifically in basophils phenocopied the healing defects observed in basophil-deficient mice, and this could be rescued by local cytokine administration.
conclusionOur study uncovers a novel pro-repair function of basophils in sensitizer-exposed skin. Beyond their well-known role in provoking itch and inflammation, basophils are critical for initiating type 2 immune-mediated tissue regeneration via IL-4/IL-13-dependent macrophage reprogramming. This axis represents a promising therapeutic target for chronic wounds, particularly in the context of allergic skin disorders.
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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 Socratic graph.