ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2020
Protective role of Galectin-7 for skin barrier impairment in atopic dermatitis.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical Effectiveness, Clinical Stability, and Effects on Serum Galectin-7 Levels of Dupilumab and JAK Inhibitors in Moderate-to-Severe Atopic Dermatitis: A Real-World, Single-Center Analysis.Medicina (Kaunas, Lithuania) · 2025Article
- What is "eczema"?The Journal of dermatology · 2025Review
- Galectin-7 reprograms skin carcinogenesis by fostering innate immune evasive programs.Cell death and differentiation · 2023Article
- Functions and Inhibition of Galectin-7, an Emerging Target in Cellular Pathophysiology.Biomolecules · 2021Review
- Diagnostic Tools and Biomarkers for Severe Drug Eruptions.International journal of molecular sciences · 2021Review
- Medawar's PostEra: Galectins Emerged as Key Players During Fetal-Maternal Glycoimmune Adaptation.Frontiers in immunology · 2021Review
- Protective role of Galectin-7 for skin barrier impairment in atopic dermatitis.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtopic dermatitis (AD) patients have a barrier disorder in association with Th2 dominant skin inflammation. Galectin-7 (Gal-7), a soluble unglycosylated lectin, is highly expressed in the stratum corneum of AD patients. However, the biological significance of increased Gal-7 expression in AD skin lesions remains unclear.
objectiveWe aimed to investigate the production mechanism and functional role of Gal-7 in AD patients and IL-4/IL-13-stimulated epidermal keratinocytes.
methodsWe assessed the Gal-7 expression levels in skin lesions and sera from AD patients. Gal-7 levels were also measured in monolayered normal human epidermal keratinocytes (NHEKs) and 3-dimensional (3D)-reconstructed epidermis in the presence or absence of IL-4/IL-13 with or without Stat3, Stat6 or Gal-7 gene silencing.
resultsGal-7 was highly expressed in the stratum corneum or intercellular space of AD lesional epidermis as assessed by the stratum corneum proteome analysis and immunohistochemistry. A positive correlation was noted between serum Gal-7 level and transepidermal water loss in patients with AD. These clinical findings were corroborated by our in vitro data, which showed that IL-4/IL-13 facilitated the extracellular release of endogenous Gal-7 in both monolayered NHEKs and 3D-reconstructed epidermis. This machinery was caused by IL-4/IL-13-induced cell damage and inhibited by knockdown of Stat6 but not Stat3 in NHEKs. Moreover, we performed Gal-7 knockdown experiment on 3D-reconstructed epidermis and the result suggested that endogenous Gal-7 serves as a protector from IL-4/IL-13-induced disruption of cell-to-cell adhesion and/or cell-to-extracellular matrix adhesion. CONCLUSION AND CLINICAL RELEVANCE: Our study unveils the characteristic of Gal-7 and its possible role as an alarmin that reflects the IL-4/IL-13-induced skin barrier impairment in AD.
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