P31 Epigenetic control of epidermal barrier function is perturbed by cutaneous inflammation

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ID: 318421
2026
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Abstract
Abstract Introduction and aims Atopic dermatitis (AD) is characterized by epidermal barrier dysfunction and immune dysregulation, with T-cell-derived type 2 immunity being hallmarks. Our previous work, suggested that an atopic environment alters keratinocyte epigenetic states, showing T helper (Th)2 inflammation perturbed keratinocyte transcriptomic phenotypes and is stable even after disease resolution. Importantly, the atopic keratinocyte immunophenotype was only ablated by blockade of Th2 signalling using anti-interleukin (IL)4RA dupilumab therapy. This suggests altered epigenetic mechanisms native to the skin itself. The purpose of this study was to investigate epigenetic alterations via methylation activity in patient-derived biopsies from lesional and nonlesional sites before and after immunomodulatory treatment. Methods We performed immunohistochemistry (IHC) on pre- and post-treatment fixed-formalin paraffin-embedded skin biopsies from lesional and nonlesional sites from 20 patients. We stained for the methylation mark known to canonically repress epidermal differentiation genes, H3K27me3, and its methyltransferase (EZH2) and demethylase (JMJD3). Results We observed an increased proportion epidermal cells expressing EZH2 in AD skin, both at lesional and nonlesional sites compared with healthy control skin, particularly within the suprabasal epidermis. This indicates ectopic expression of EZH2 outside the canonical basal compartment of the epidermis. Post-treatment (16 ± 2 weeks) the fraction of EZH2-poisitive cells in the lesional epidermis was stable; however, the overall expression level of positive cells was comparable to healthy epidermis when measured using an H-score index. However, both lesional and nonlesional epidermis experienced a post-treatment loss of H3K27me3, which was not entirely explained by loss of EZH2 but overexpression of JMJD3 demethylase. Conclusions Our IHC data suggest that epigenetic regulation epidermal differentiation is altered by atopic inflammation, and treatment-induced lesion clearance does not result in a return to healthy phenotype, i.e. loss of the H3K27me3 mark is characteristic of nonlesional but not healthy skin. Future work aims to locate the specific gene loci involved in EZH2/JMJD3 regulation in the context of active and resolved cutaneous atopic inflammation.
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Authors Kalum Clayton, Naipapon Chupreecha, Purevsuren Losol, Michael Ardern-Jones
Journal the british journal of dermatology
Year 2026
DOI
10.1093/bjd/ljag151.070
URL
https://doi.org/10.1093/bjd/ljag151.070
Keywords Keywords not found

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