ArticleCell reports2019
Single-Cell Analysis Suggests that Ongoing Affinity Maturation Drives the Emergence of Pemphigus Vulgaris Autoimmune Disease.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- B-cell centrality dictates therapeutic efficacy across autoimmune diseases: a systematic review.Frontiers in immunology · 2026Pooled it
- FcRn Antagonism Leads to a Decrease of Desmoglein-Specific B Cells: Secondary Analysis of a Phase 2 Study of Efgartigimod in Pemphigus Vulgaris and Pemphigus Foliaceus.Frontiers in immunology · 2022Trial
- Article
- Anti-interferon-γ autoantibodies: immunopathogenesis, diagnostic innovation, and emerging therapeutic strategies in an adult-onset immunodeficiency.Frontiers in immunology · 2026Review
- Pemphigus Vulgaris Autoantibodies Induce an Endoplasmic Reticulum Stress Response.The Journal of investigative dermatology · 2025Article
- 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
- Identification of distinct epitopes in dipeptidyl peptidase-4 inhibitor-associated bullous pemphigoid.Science advances · 2025Article
- De novo antibody identification in human blood from full-length single B cell transcriptomics and matching haplotype-resolved germline assemblies.Genome research · 2025Article
- Antidesmoglein 1 and 3 serum IgG and positivity by direct immunofluorescence microscopy is associated with relapse in pemphigus in a prospective bicontinental study.JAAD international · 2025Article
- Immunostimulatory effects of Toll-like receptor ligands as adjuvants in establishing a novel mouse model for pemphigus vulgaris.Clinical and translational medicine · 2024Article
- IgG reactivity to different desmoglein-3 ectodomains in pemphigus vulgaris: novel panels for assessing disease severity.Frontiers in immunology · 2024Article
- Plasma Exosomal microRNA Profile Reveals miRNA 148a-3p Downregulation in the Mucosal-Dominant Variant of Pemphigus Vulgaris.International journal of molecular sciences · 2023Article
- B-cell targeted therapy of pemphigus.The Journal of dermatology · 2023Review
- Understanding CD4Frontiers in immunology · 2023Review
- Pemphigus: trigger and predisposing factors.Frontiers in medicine · 2023Review
- Pemphigus and Pemphigoid: From Disease Mechanisms to Druggable Pathways.The Journal of investigative dermatology · 2022Review
- Immunopathology and Immunotherapy of Inflammatory Skin Diseases.Immune network · 2022Review
- The Diversity of Serum Anti-DSG3 IgG Subclasses Has a Major Impact on Pemphigus Activity and Is Predictive of Relapses After Treatment With Rituximab.Frontiers in immunology · 2022Article
- Clinical impact and a prognostic marker of early rituximab treatment after rituximab reimbursement in Korean pemphigus patients.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
Abstract
Pemphigus vulgaris (PV) is an autoimmune disease characterized by blistering sores on skin and mucosal membranes, caused by autoantibodies primarily targeting the cellular adhesion protein, desmoglein-3 (Dsg3). To better understand how Dsg3-specific autoantibodies develop and cause disease in humans, we performed a cross-sectional study of PV patients before and after treatment to track relevant cellular responses underlying disease pathogenesis, and we provide an in-depth analysis of two patients by generating a panel of mAbs from single Dsg3-specific memory B cells (MBCs). Additionally, we analyzed a paired sample from one patient collected 15-months prior to disease diagnosis. We find that Dsg3-specific MBCs have an activated phenotype and show signs of ongoing affinity maturation and clonal selection. Monoclonal antibodies (mAbs) with pathogenic activity primarily target epitopes in the extracellular domains EC1 and EC2 of Dsg3, though they can also bind to the EC4 domain. Combining antibodies targeting different epitopes synergistically enhances in vitro pathogenicity.
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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.