Evidence map›Paper›PMID 41074677›Full record

ArticleAllergy2026

Basophils in Skin-Mediated Sensitization Drive Subsequent Lung Inflammation in Airway-Challenged Mice.

E Da Choi, David Voehringer, Daniel Radtke

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

E Da ChoiDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU), Erlangen, Germany.ORCID 0009-0007-9941-4578
David VoehringerDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU), Erlangen, Germany.ORCID 0000-0001-6650-0639
Daniel RadtkeDepartment of Infection Biology, University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU), Erlangen, Germany.ORCID 0000-0003-3241-4542

Funding

Deutsche ForschungsgemeinschaftInterdisziplinäres Zentrum für Klinische Forschung, Universitätsklinikum Erlangen
6 · The paper itself

Abstract

backgroundAtopic dermatitis (AD) and asthma are observed as epidemiologically linked allergic comorbidities, both characterized by elevated systemic IgE levels and type 2 immunity. Basophils play a pivotal role in these responses by producing interleukin-4 (IL-4), which is essential for IgE synthesis and allergic inflammation. However, their specific impact on the progression from AD to asthma remains unclear.

methodsWe utilized an AD model in basophil-deficient Mcpt8Cre mice and temporarily basophil-depleted mice, where topical application of the vitamin D analog MC903 induced the alarmin TSLP, resulting in AD-like symptoms. In addition, we topically applied ovalbumin (OVA) as a model allergen to trace the allergen-specific immune response. We determined allergen-specific antibody formation by analysis of the germinal center reaction and measured serum antibody concentrations and IgE loading of basophils in the spleen and lung. We further challenged mice sensitized via the skin in anaphylaxis and allergic lung inflammation models.

resultsOur results demonstrate that basophils promote loss of skin barrier integrity, allergen-specific IgE formation, and subsequent allergic responses. Basophil depletion selectively during sensitization significantly reduced IgE-dependent anaphylaxis and lung inflammation. In challenged lungs, reduced inflammation and eosinophilia were accompanied by lower levels of chemokines CCL17 and CCL24, which attract Th2 cells and eosinophils, respectively. Notably, Il4 and Il13 were not affected by basophil depletion during sensitization but were reduced in mice that permanently lack basophils.

conclusionWe find that basophils promote IgE formation and lung sensitization to skin-encountered allergens and drive secondary allergen-induced lung inflammation. We separate the role of basophils in sensitization from their effector function during anaphylaxis or lung inflammation relevant to envision novel strategies to prevent the development of allergic comorbidities.

Indexed as

BasophilsDermatitis, AtopicPneumoniaSkinAllergensAnaphylaxisAnimalsAsthmaCytokinesDisease Models, AnimalImmunizationImmunoglobulin EMiceOvalbuminAllergensCytokinesImmunoglobulin EOvalbuminanaphylaxisbasophilIgElungsensitization

Identifiers

PMID41074677
PMCPMC12773652

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.