ArticleProceedings of the National Academy of Sciences of the United States of America2016
Multiplexed autoantigen microarrays identify HLA as a key driver of anti-desmoglein and -non-desmoglein reactivities in pemphigus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 56 citations in OpenAlex.
- Data-driven image analysis to determine antibody-induced dissociation of cell-cell adhesion and antibody pathogenicity in pemphigus.PNAS nexus · 2025Article
- 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
- Cytokine profiling reveals HLA-linked Th2 and Th17 driven immune activation in pemphigus vulgaris patients and genetically susceptible healthy controls.Frontiers in immunology · 2024Article
- Healthy individuals genetically at-risk for the development of Pemphigus vulgaris or Alopecia areata share disease-like cytokine dysregulation.Frontiers in immunology · 2024Article
- Quality-controlled characterization of a monoclonal antibody specific to an EC5-domain of human desmoglein 3 for pemphigus research.Frontiers in immunology · 2024Article
- Article
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Case report: Documentation of cutaneous only pemphigus vulgaris without history of mucosal lesions in North America.Frontiers in immunology · 2022Article
- Patient genetics shape the autoimmune response in the blistering skin disease pemphigus vulgaris.Frontiers in immunology · 2022Article
- Desmoglein compensation hypothesis fidelity assessment in Pemphigus.Frontiers in immunology · 2022Article
- The Immunogenetics of Autoimmune Blistering Diseases.Advances in experimental medicine and biology · 2022Review
- Modulation of Mechanical Stress Mitigates Anti-Dsg3 Antibody-Induced Dissociation of Cell-Cell Adhesion.Advanced biology · 2021Article
- Beyond the HLA polymorphism: A complex pattern of genetic susceptibility to pemphigus.Genetics and molecular biology · 2020Article
- Article
- Synergy among non-desmoglein antibodies contributes to the immunopathology of desmoglein antibody-negative pemphigus vulgaris.The Journal of biological chemistry · 2019Article
- Role of Dsg1- and Dsg3-Mediated Signaling in Pemphigus Autoantibody-Induced Loss of Keratinocyte Cohesion.Frontiers in immunology · 2019Article
- Editorial: Autoantibodies.Frontiers in immunology · 2019Article
- Anti-Thyroid Peroxidase Reactivity Is Heightened in Pemphigus Vulgaris and Is Driven by Human Leukocyte Antigen Status and the Absence of Desmoglein Reactivity.Frontiers in immunology · 2018Article
- Immunoadsorption of Desmoglein-3-Specific IgG Abolishes the Blister-Inducing Capacity of Pemphigus Vulgaris IgG in Neonatal Mice.Frontiers in immunology · 2018Article
- The Evolving Story of Autoantibodies in Pemphigus Vulgaris: Development of the "Super Compensation Hypothesis".Frontiers in medicine · 2018Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with pemphigus vulgaris (PV) harbor antibodies reactive against self-antigens expressed at the surface of keratinocytes, primarily desmoglein (Dsg) 3 and, to a lesser extent, Dsg1. Conventionally, only antibodies targeting these molecules have been thought to contribute to disease pathogenesis. This notion has been challenged by a growing pool of evidence that suggests that antibodies toward additional targets may play a role in disease. The aims of this study were to (i) establish high-throughput protein microarray technology as a method to investigate traditional and putative autoantibodies (autoAbs) in PV and (ii) use multiplexed protein array technology to define the scope and specificity of the autoAb response in PV. Our analysis demonstrated significant IgG reactivity in patients with PV toward the muscarinic acetylcholine receptor subtypes 3, 4, and 5 as well as thyroid peroxidase. Furthermore, we found that healthy first- and second-degree relatives of patients with PV express autoAbs toward desmoglein and non-Dsg targets. Our analysis also identified genetic elements, particularly HLA, as key drivers of autoAb expression. Finally, we show that patients with PV exhibit significantly reduced IgM reactivity toward disease-associated antigens relative to controls. The use of protein microarrays to profile the autoAb response in PV advanced the current understanding of disease and provided insight into the complex relationship between genetics and disease development.
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