ArticleThe Journal of clinical investigation2013
Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 97 citations in OpenAlex.
- Plakoglobin phosphorylation at serine 665 is capable of stabilizing cadherin-mediated adhesion in keratinocytes.JCI insight · 2026Article
- Inhibition of the JAK/STAT Signaling Pathway Suggests a Protective Effect against Acantholysis in Pemphigus.Inflammation · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Novel Serum Oxidative Stress Biomarkers in Pemphigus Vulgaris: Clinical Insights and Implications for Pathogenesis.Dermatology practical & conceptual · 2025Article
- Research progress on bioactive peptides in the treatment of oral diseases.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- Meeting report - Alpine desmosome disease meeting 2024: advances and emerging topics in desmosomes and related diseases.Journal of cell science · 2025Article
- Adhesion of pancreatic tumor cell clusters by desmosomal molecules enhances early liver metastases formation.Scientific reports · 2024Article
- Role of auto-antibodies in the mechanisms of dengue pathogenesis and its progression: a comprehensive review.Archives of microbiology · 2024Review
- The impact of signaling pathways on the desmosome ultrastructure in pemphigus.Frontiers in immunology · 2024Article
- Structure and regulation of desmosomes in intercalated discs: Lessons from epithelia.Journal of anatomy · 2023Review
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023Article
- Desmoglein 2 can undergo CaBiophysical journal · 2022Article
- Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022Review
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Unmet Medical Needs in Chronic, Non-communicable Inflammatory Skin Diseases.Frontiers in medicine · 2022Review
- Role of ADAM10 and ADAM17 in the Regulation of Keratinocyte Adhesion in Pemphigus Vulgaris.Frontiers in immunology · 2022Article
- Cadherin Signaling in Cancer and Autoimmune Diseases.International journal of molecular sciences · 2021Review
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Identification of novel therapeutic targets for blocking acantholysis in pemphigus.British journal of pharmacology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In pemphigus vulgaris, a life-threatening autoimmune skin disease, epidermal blisters are caused by autoantibodies primarily targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratinocyte cohesion. Due to limited insights into disease pathogenesis, current therapy relies primarily on nonspecific long-term immunosuppression. Both direct inhibition of DSG transinteraction and altered intracellular signaling by p38 MAPK likely contribute to the loss of cell adhesion. Here, we applied a tandem peptide (TP) consisting of 2 connected peptide sequences targeting the DSG adhesive interface that was capable of blocking autoantibody-mediated direct interference of DSG3 transinteraction, as revealed by atomic force microscopy and optical trapping. Importantly, TP abrogated autoantibody-mediated skin blistering in mice and was effective when applied topically. Mechanistically, TP inhibited both autoantibody-induced p38 MAPK activation and its association with DSG3, abrogated p38 MAPK-induced keratin filament retraction, and promoted desmosomal DSG3 oligomerization. These data indicate that p38 MAPK links autoantibody-mediated inhibition of DSG3 binding to skin blistering. By limiting loss of DSG3 transinteraction, p38 MAPK activation, and keratin filament retraction, which are hallmarks of pemphigus pathogenesis, TP may serve as a promising treatment option.
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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.