ArticleImmunity, inflammation and disease2021
IL-13 modulates ∆Np63 levels causing altered expression of barrier- and inflammation-related molecules in human keratinocytes: A possible explanation for chronicity of atopic dermatitis.
Article in Immunity, inflammation and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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11 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Keratinocytes as active regulators of cutaneous and mucosal immunity: a systematic review across inflammatory epithelial disorders.Frontiers in immunology · 2025Pooled it
- DAPL1 is activated by Np63 and GRα and regulates lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Extracellular vesicles modulate skin aging biomarkers in a 3D reconstructed full-thickness skin model.Frontiers in cell and developmental biology · 2026Article
- Targeting NLRP10 in Atopic Dermatitis: An Emerging Strategy to Modulate Epidermal Cell Death and Barrier Function.International journal of molecular sciences · 2025Review
- NLRP10 maintains epidermal homeostasis by promoting keratinocyte survival and P63-dependent differentiation and barrier function.Cell death & disease · 2024Article
- Development of new dehydrocostuslactone derivatives for treatment of atopic dermatitisRSC medicinal chemistry · 2024Article
- Characterization of the Pro-Inflammatory and Pruritogenic Transcriptome in Skin Lesions of the Experimental Canine Atopic Acute IgE-Mediated Late Phase Reactions Model and Correlation to Acute Skin Lesions of Human Atopic Dermatitis.Veterinary sciences · 2024Article
- Generation of self-replicating airway organoids from the cave nectar batEmerging microbes & infections · 2023Article
- Type 2 inflammation drives an airway basal stem cell program through insulin receptor substrate signaling.The Journal of allergy and clinical immunology · 2023Article
- Cisplatin-induced HSF1-HSP90 axis enhances the expression of functional PD-L1 in oral squamous cell carcinoma.Cancer medicine · 2023Article
- IL-13 modulates ∆Np63 levels causing altered expression of barrier- and inflammation-related molecules in human keratinocytes: A possible explanation for chronicity of atopic dermatitis.Immunity, inflammation and disease · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundBarrier disruption and an excessive immune response in keratinocytes are now considered to have important roles in the pathophysiology of atopic dermatitis (AD). Furthermore, disturbed keratinocyte differentiation is considered to underlie AD. ΔNp63, a p53-like transcription factor, is a major regulator of keratinocyte differentiation. However, the functional significance of ΔNp63 in AD has not been clarified.
objectiveIn this study, we aimed to investigate the influence of the type 2 inflammatory environment on ΔNp63 expression and AD-associated molecules regulated by ΔNp63 in keratinocytes.
methodsThe immunohistochemical expression profiles of ΔNp63 and AD-related molecules were evaluated in human skin tissue. The function of ΔNp63 in the regulation of AD-related molecules and the influence of the type 2 inflammatory environment on ΔNp63 expression were investigated using human primary keratinocytes. Expression of ΔNp63 was manipulated using the RNA interfering method.
resultsIn healthy skin tissue, we observed an inverse expression pattern between ∆Np63 and some barrier-related proteins including filaggrin, caspase-14, claudin-1, and claudin-4. ΔNp63 regulated expression of these genes and proteins. In addition, production of IL-1β and IL-33, pro-inflammatory cytokines, was modulated by ΔNp63. Furthermore, prolonged IL-13 exposure increased the thickness of the three-dimensional culture of keratinocytes. IL-13 interfered with ΔNp63 downregulation during calcium-induced keratinocyte differentiation. IL-13 modulated some barrier-related and inflammation-related molecules, which were regulated by ΔNp63.
conclusionsWe have shown that ΔNp63 modulated AD-related barrier and inflammatory molecules. In addition, ΔNp63 expression was affected by IL-4/IL-13. IL-13-ΔNp63 axis would integrate two major factors of AD pathogenesis: dysregulated barrier and inflammation.
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