ArticleThe Journal of investigative dermatology2009
Disruption of desmosome assembly by monovalent human pemphigus vulgaris monoclonal antibodies.
Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 70 citations in OpenAlex.
- MiR-125b-5p promotes pemphigus vulgaris pathogenesis by modulating desmosome structures.Bioscience reports · 2026Article
- Caspase-activation powers anti-Desmoglein 3-induced acantholysis in human epidermis.Cell death discovery · 2026Article
- Dsg3 epitope-specific signalling in pemphigus.Frontiers in immunology · 2023Article
- In Vitro, Ex Vivo, and In Vivo Models for the Study of Pemphigus.International journal of molecular sciences · 2022Review
- Pemphigus Vulgaris: Present and Future Therapeutic Strategies.Dermatology practical & conceptual · 2022Review
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- The pathogenesis of bullous skin diseases.Journal of translational autoimmunity · 2019Review
- Pemphigus: Current and Future Therapeutic Strategies.Frontiers in immunology · 2019Review
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- RPGRIP1L is required for stabilizing epidermal keratinocyte adhesion through regulating desmoglein endocytosis.PLoS genetics · 2019Article
- Pathogenic IgG4 autoantibodies from endemic pemphigus foliaceus recognize a desmoglein-1 conformational epitope.Journal of autoimmunity · 2018Article
- Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice.Frontiers in immunology · 2018Article
- Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.Frontiers in immunology · 2018Review
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- Pemphigus-A Disease of Desmosome Dysfunction Caused by Multiple Mechanisms.Frontiers in immunology · 2018Review
- Pemphigus.Nature reviews. Disease primers · 2017Review
- Stat3 regulates desmoglein 3 transcription in epithelial keratinocytes.JCI insight · 2017Article
- Setting the target for pemphigus vulgaris therapy.JCI insight · 2017Review
- Determinants of VH1-46 Cross-Reactivity to Pemphigus Vulgaris Autoantigen Desmoglein 3 and Rotavirus Antigen VP6.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Mechanisms of Disease: Pemphigus and Bullous Pemphigoid.Annual review of pathology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The intercellular interactions of the desmosomal cadherins, desmoglein and desmocollin, are required for epidermal cell adhesion. Pemphigus vulgaris (PV) is a potentially fatal autoimmune blistering disease characterized by autoantibodies against desmoglein (Dsg) 3. During calcium-induced desmosome assembly, treatment of primary human keratinocytes with pathogenic monovalent anti-Dsg3 mAbs produced from a PV patient causes a decrease of Dsg3 and desmoplakin but not desmocollin (Dsc) 3 in the Triton-insoluble fraction of cell lysates within 2 hours. Immunofluorescence and antibody ELISA studies suggest that pathogenic mAbs cause internalization of cell-surface Dsg3 but not Dsc3 through early endosomes. Electron microscopy demonstrated a lack of well-formed desmosomes in keratinocytes treated with pathogenic compared to nonpathogenic mAbs. In contrast, pathogenic mAbs caused late depletion of Dsg3 from preformed desmosomes at 24 hours, with effects on multiple desmosomal proteins including Dsc3 and plakoglobin. Together, these studies indicate that pathogenic PV mAbs specifically cause internalization of newly synthesized Dsg3 during desmosome assembly, correlating with their pathogenic activity. Monovalent human PV anti-Dsg mAbs reproduce the effects of polyclonal PV IgG on Dsg3 and will facilitate future studies to further dissect the cellular mechanisms for the loss of cell adhesion in pemphigus.
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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.