ArticleThe Journal of allergy and clinical immunology2025
Identification of disease-specific regulatory networks in prurigo nodularis versus atopic dermatitis through ATAC/RNA single-nucleus profiling.
Article in The Journal of allergy and clinical immunology, 2025. 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
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Who cites it
2 citing papers in PubMed.
- Epithelial-Dermal Immune Memory: TrackingInternational journal of molecular sciences · 2026Review
- Epigenetic reprogramming in autoimmune and immune-mediated skin disease.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundPrurigo nodularis (PN) is a chronic neuroimmune skin disorder characterized by chronic itch and multiple pruriginous nodules, and is related to atopic dermatitis (AD). While different transcriptomic studies have been conducted, the regulatory mechanisms and differences between PN and AD remain poorly understood.
objectiveWe aimed to uncover shared and distinct regulatory mechanisms between PN and AD. Specifically, we evaluated how molecular factors driving the distinction between lesional and nonlesional skin differ in these two diseases.
methodWe profiled gene expression and chromatin accessibility at the single-nucleus level from paired lesional and nonlesional skin samples of 4 PN patients and 5 AD patients. We utilized joint modeling and pseudobulk techniques to identify disease specific regulatory network.
resultsThe epigenomic alterations in PN were more numerous and of greater magnitude compared to AD skin. PN-biased cis-regulatory elements showed correlation with PN-biased differentially expressed genes in the same cell type, and we identified 199 regulatory modules specific to PN, in contrast to 3 modules specific to AD. We also identified PN-specific AP-1-induced regulatory module that induces RUNX2 in fibroblasts, confirmed by immunohistochemistry and immunofluorescence staining, suggestive of its contribution to fibrosis in PN.
conclusionThis study provides a chromatin RNA expression atlas and underscores its efficacy in revealing distinct regulatory mechanisms inherent to PN and AD.
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