ArticleAllergy2026
Integrated Methylome-Transcriptome Analysis Reveals Epigenomic Remodeling and Rho GTPase-Linked Immune-Epithelial Crosstalk in Atopic Dermatitis.
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.
- Article
- Epigenetic reprogramming in autoimmune and immune-mediated skin disease.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundAtopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation and epithelial barrier dysfunction. Although transcriptional changes in AD skin are increasingly well characterized, DNA methylation patterns remain less well understood.
methodsHere, we present an integrated analysis of matched DNA methylomes, transcriptomes, and microbiomes from lesional (n = 40), adjacent non-lesional (n = 38), and healthy control (n = 40) skin, using complementary cell-type-adjusted models.
resultsWe identified thousands of differentially methylated regions (DMRs) across all pairwise contrasts (lesional vs. healthy: n = 13,514; lesional vs. non-lesional: n = 4591; non-lesional vs. healthy: n = 1716), including both hyper- and hypo-methylated regions with balanced effect sizes. A core subset of DMRs persisted after methylation-based adjustment, whereas the extensive lesional vs. non-lesional set was largely composition-driven. Integration with transcriptomic co-expression networks linked DMRs to immune-epithelial modules, and 225 DMR-gene pairs showed significant anti-correlation (FDR < 0.05). Lesional skin with dominant Staphylococcus aureus colonization differed at 92 DMRs compared with absent-colonized skin, of which 70 also overlapped with local severity. Pathway analyses consistently highlighted Rho GTPase and actin-junctional programs across analytic layers, suggesting that Rho GTPase signaling is a central integrator of immune, epithelial, and microbial interactions in AD.
conclusionsOur study underscores the importance of epigenomic remodeling in AD and highlights potential avenues for precision intervention in chronic inflammatory skin disease.
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Registered trials
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