ArticleFrontiers in immunology2026
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by type-2-mediated inflammation, along with the detection of type-1 and type-3 cytokines in lesional skin. The skin microbiome of lesional skin is dominated by the pathogen Methods: Specific serum IgE against Spl family members was quantified, and SplB-specific CD4 Results: We observed significantly elevated levels of IgE antibodies specific for Spl family proteins in patients with AD compared to healthy controls. Discussion: The presence of clonally propagated SplB-specific T cells in the skin of patients with AD strongly suggests an impact on inflammation. This type of cellular immune response, which is not exclusively polarized towards type 2, reflects the AD phenotype. This suggests that the adaptive immune response to S. aureus contributes to this phenotype.
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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.