ArticleNature communications2014
Shared VH1-46 gene usage by pemphigus vulgaris autoantibodies indicates common humoral immune responses among patients.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Characteristics of anti-integrin αvβ6 autoantibodies in patients with ulcerative colitis.JCI insight · 2026Article
- Individual myasthenia gravis autoantibody clones can efficiently mediate multiple mechanisms of pathology.Acta neuropathologica · 2023Article
- T cell autoimmunity and immune regulation to desmoglein 3, a pemphigus autoantigen.The Journal of dermatology · 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
- Clinical impact and a prognostic marker of early rituximab treatment after rituximab reimbursement in Korean pemphigus patients.Frontiers in immunology · 2022Article
- An Immunoproteomic Survey of the Antibody Landscape: Insights and Opportunities Revealed by Serological Repertoire Profiling.Frontiers in immunology · 2022Review
- Article
- A three-body affair.Nature nanotechnology · 2020Article
- Walnut antigens can trigger autoantibody development in patients with pemphigus vulgaris through a "hit-and-run" mechanism.The Journal of allergy and clinical immunology · 2019Article
- Single-Cell Analysis Suggests that Ongoing Affinity Maturation Drives the Emergence of Pemphigus Vulgaris Autoimmune Disease.Cell reports · 2019Article
- Characterization of pathogenic monoclonal autoantibodies derived from muscle-specific kinase myasthenia gravis patients.JCI insight · 2019Article
- Autoreactive IgG and IgA B Cells Evolve through Distinct Subclass Switch Pathways in the Autoimmune Disease Pemphigus Vulgaris.Cell reports · 2018Article
- Pemphigus: a Comprehensive Review on Pathogenesis, Clinical Presentation and Novel Therapeutic Approaches.Clinical reviews in allergy & immunology · 2018Review
- Recent advances in the understanding and treatment of pemphigus and pemphigoid.F1000Research · 2018Review
- Antibody Repertoire Analysis of Hepatitis C Virus Infections Identifies Immune Signatures Associated With Spontaneous Clearance.Frontiers in immunology · 2018Article
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- VDJ gene usage among B-cell receptors in ABO-incompatible kidney transplantation determined by RNA-seq Transcriptomic analysis.BMC nephrology · 2017Article
- Pemphigus.Nature reviews. Disease primers · 2017Review
- Setting the target for pemphigus vulgaris therapy.JCI insight · 2017Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
Pemphigus vulgaris (PV) is a potentially fatal blistering disease caused by autoantibodies (autoAbs) against desmoglein 3 (Dsg3). Here, we clone anti-Dsg3 antibodies (Abs) from four PV patients and identify pathogenic VH1-46 autoAbs from all four patients. Unexpectedly, VH1-46 autoAbs had relatively few replacement mutations. We reverted antibody somatic mutations to their germline sequences to determine the requirement of mutations for autoreactivity. Three of five VH1-46 germline-reverted Abs maintain Dsg3 binding, compared with zero of five non-VH1-46 germline-reverted Abs. Site-directed mutagenesis of VH1-46 Abs demonstrates that acidic amino-acid residues introduced by somatic mutation or heavy chain VDJ recombination are necessary and sufficient for Dsg3 binding. Our data suggest that VH1-46 autoantibody gene usage is commonly found in PV because VH1-46 Abs require few to no mutations to acquire Dsg3 autoreactivity, which may favour their early selection. Common VH gene usage indicates common humoral immune responses, even among unrelated patients.
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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.