ArticleLife (Basel, Switzerland)2021
Ex-Vivo Skin Explant Culture Is a Model for TSLP-Mediated Skin Barrier Immunity.
Article in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Amphibian-derived peptides as novel therapeutics for skin wound healing: Mechanisms, applications, and challenges.Zoological research · 2026Review
- Skin-on-chip: Quo vadis?APL bioengineering · 2025Review
- Vitamin K supports TGF-β1 dependedFrontiers in immunology · 2025Article
- JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia.EMBO molecular medicine · 2024Article
- The Development of Human Ex Vivo Models of Inflammatory Skin Conditions.International journal of molecular sciences · 2023Article
- NF-κB signaling pathway mechanism in cow intertoe skin inflammation caused byFrontiers in cellular and infection microbiology · 2023Article
- BMPR1a Is Required for the Optimal TGFβ1-Dependent CD207The Journal of investigative dermatology · 2022Article
- Immuno-Pathogenesis of Chronic Inflammatory Skin Diseases: Novel Molecular Targets and Biomarkers.Life (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The skin is the outermost barrier protecting the body from pathogenic invasion and environmental insults. Its breakdown initiates the start of skin inflammation. The epidermal growth factor (EGFR) on keratinocytes protects this barrier, and its dysfunction leads to atopic dermatitis-like skin disease. One of the initial cytokines expressed upon skin barrier breach and during atopic dermatitis is TSLP. Here, we describe the expression and secretion of TSLP during EGFR inhibition and present an ex-vivo model, which mimics the early events after barrier insult. Skin explants floated on culture medium at 32 °C released TSLP in parallel to the activation of the resident Langerhans cell network. We could further show the up-regulation and activation of the AP-1 family of transcription factors during atopic-like skin inflammation and its involvement in TSLP production from the skin explant cultures. Inhibition of the c-Jun N-terminal kinase pathway led to a dose-dependent blunting of TSLP release. These data indicate the involvement of AP-1 during the early stages of atopic-like skin inflammation and highlight a novel therapeutic approach by targeting it. Therefore, skin explant cultures mimic the early events during skin barrier immunity and provide a suitable model to test therapeutic intervention.
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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.