ReviewFrontiers in immunology2018
Autoantibody Signaling in Pemphigus Vulgaris: Development of an Integrated Model.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 40 citations in OpenAlex.
- Protocol to quantify desmoglein 3 tension at cell-cell adhesions using FRET-based tension sensors.STAR protocols · 2026Article
- Article
- Antigen-Fc fusion therapy reduces severity of a model of pemphigus vulgaris without systemic immunosuppression.Science translational medicine · 2025Article
- Desmosomal cadherin tension loss in pemphigus vulgaris mediated by the inhibition of active RhoA at cell-cell adhesions.iScience · 2025Article
- Novel Serum Oxidative Stress Biomarkers in Pemphigus Vulgaris: Clinical Insights and Implications for Pathogenesis.Dermatology practical & conceptual · 2025Article
- APLAID complicated with arrhythmogenic dilated cardiomyopathy caused by a novel PLCG2 variant.Immunologic research · 2024Article
- Desmosomal Cadherin Tension Loss in Pemphigus Vulgaris Mediated by the Inhibition of Active RhoA at Cell-Cell Adhesions.bioRxiv : the preprint server for biology · 2024Article
- Synthetically mannosylated antigens induce antigen-specific humoral tolerance and reduce anti-drug antibody responses to immunogenic biologics.Cell reports. Medicine · 2024Article
- Evaluation of link between COVID-19 adjacent spike in hydroxychloroquine use and increased reports of pemphigus: a disproportionality analysis of the FDA Adverse Event Reporting System.Frontiers in immunology · 2024Observational
- Treatment-naïve pemphigus patients showing IgG tissue deposits have serum IgG antibodies against desmoglein 1 detected more often than those against desmoglein 3: a monocentre laboratory experience.Postepy dermatologii i alergologii · 2023Article
- The Role of LFA-1 for the Differentiation and Function of Regulatory T Cells-Lessons Learned from Different Transgenic Mouse Models.International journal of molecular sciences · 2023Review
- Skin-infiltrating T cells display distinct inflammatory signatures in lichen planus, bullous pemphigoid and pemphigus vulgaris.Frontiers in immunology · 2023Article
- Impaired Treg-DC interactions contribute to autoimmunity in leukocyte adhesion deficiency type 1.JCI insight · 2022Article
- Spatially Guided Construction of Multilayered Epidermal Models Recapturing Structural Hierarchy and Cell-Cell Junctions.Small science · 2022Article
- Pemphigus and Pemphigoid: From Disease Mechanisms to Druggable Pathways.The Journal of investigative dermatology · 2022Review
- Marked to Die-Cell Death Mechanisms for Keratinocyte Acantholysis in Pemphigus Diseases.Life (Basel, Switzerland) · 2022Review
- Mechanisms Causing Acantholysis in Pemphigus-Lessons from Human Skin.Frontiers in immunology · 2022Review
- Evolving Mechanisms in the Pathophysiology of Pemphigus Vulgaris: A Review Emphasizing the Role of Desmoglein 3 in Regulating p53 and the Yes-Associated Protein.Life (Basel, Switzerland) · 2021Review
- Serum Detection of Anti-thyroid Peroxidase and Anti-thyroglobulin Antibodies in Chinese Patients With Pemphigus Vulgaris and Pemphigus Foliaceus and Literature Review.Frontiers in immunology · 2021Observational
- Modulation of Mechanical Stress Mitigates Anti-Dsg3 Antibody-Induced Dissociation of Cell-Cell Adhesion.Advanced biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pemphigus vulgaris (PV) is an autoimmune skin blistering disease effecting both cutaneous and mucosal epithelia. Blister formation in PV is known to result from the binding of autoantibodies (autoAbs) to keratinocyte antigens. The primary antigenic targets of pathogenic autoAbs are known to be desmoglein 3, and to a lesser extent, desmoglein 1, cadherin family proteins that partially comprise the desmosome, a protein structure responsible for maintaining cell adhesion, although additional autoAbs, whose role in blister formation is still unclear, are also known to be present in PV patients. Nevertheless, there remain large gaps in knowledge concerning the precise mechanisms through which autoAb binding induces blister formation. Consequently, the primary therapeutic interventions for PV focus on systemic immunosuppression, whose side effects represent a significant health risk to patients. In an effort to identify novel, disease-specific therapeutic targets, a multitude of studies attempting to elucidate the pathogenic mechanisms downstream of autoAb binding, have led to significant advancements in the understanding of autoAb-mediated blister formation. Despite this enhanced characterization of disease processes, a satisfactory explanation of autoAb-induced acantholysis still does not exist. Here, we carefully review the literature investigating the pathogenic disease mechanisms in PV and, taking into account the full scope of results from these studies, provide a novel, comprehensive theory of blister formation in PV.
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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.