ArticleThe Journal of clinical investigation2010
Homologous regions of autoantibody heavy chain complementarity-determining region 3 (H-CDR3) in patients with pemphigus cause pathogenicity.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 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
- Oral Lesions in Autoimmune Bullous Diseases: An Overview of Clinical Characteristics and Diagnostic Algorithm.American journal of clinical dermatology · 2019Review
- Single-Cell Analysis Suggests that Ongoing Affinity Maturation Drives the Emergence of Pemphigus Vulgaris Autoimmune Disease.Cell reports · 2019Article
- Autoreactive IgG and IgA B Cells Evolve through Distinct Subclass Switch Pathways in the Autoimmune Disease Pemphigus Vulgaris.Cell reports · 2018Article
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- Recent advances in the understanding and treatment of pemphigus and pemphigoid.F1000Research · 2018Review
- Pemphigus.Nature reviews. Disease primers · 2017Review
- Proteomic Analysis of Pemphigus Autoantibodies Indicates a Larger, More Diverse, and More Dynamic Repertoire than Determined by B Cell Genetics.Cell reports · 2017Article
- Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017Review
- Article
- Non-infectious environmental antigens as a trigger for the initiation of an autoimmune skin disease.Autoimmunity reviews · 2016Review
- Mechanisms of Disease: Pemphigus and Bullous Pemphigoid.Annual review of pathology · 2016Review
- Overlapping IgG4 Responses to Self- and Environmental Antigens in Endemic Pemphigus Foliaceus.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Immune response in pemphigus and beyond: progresses and emerging concepts.Seminars in immunopathology · 2016Review
- Critical Role of the Neonatal Fc Receptor (FcRn) in the Pathogenic Action of Antimitochondrial Autoantibodies Synergizing with Anti-desmoglein Autoantibodies in Pemphigus Vulgaris.The Journal of biological chemistry · 2015Article
- Restricted, canonical, stereotyped and convergent immunoglobulin responses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- The analysis of clonal expansions in normal and autoimmune B cell repertoires.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Review
- Persistence of anti-desmoglein 3 IgG(+) B-cell clones in pemphigus patients over years.The Journal of investigative dermatology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Pemphigus is a life-threatening autoimmune disease in which antibodies specific for desmogleins (Dsgs) cause loss of keratinocyte cell adhesion and blisters. In order to understand how antibodies cause pathogenicity and whether there are commonalities among antibodies in different patients that could ultimately be used to target specific therapy against these antibodies, we characterized Dsg-specific mAbs cloned by phage display from 3 patients with pemphigus vulgaris and 2 with pemphigus foliaceus. Variable heavy chain gene usage was restricted, but similar genes were used for both pathogenic and nonpathogenic mAbs. However, the heavy chain complementarity-determining region 3 (H-CDR3) of most pathogenic, but not nonpathogenic, mAbs shared an amino acid consensus sequence. Randomization of the H-CDR3 and site-directed mutagenesis indicated that changes in this sequence could block pathogenicity but not necessarily binding. In addition, for 2 antibodies with longer H-CDR3s, a tryptophan was critical for pathogenicity but not binding, a result that is consistent with blocking the tryptophan acceptor site that is thought to be necessary for Dsg-mediated adhesion. These studies indicate that H-CDR3 is critical for pathogenicity of a human autoantibody, that a small region (even 1 amino acid) can mediate pathogenicity, and that pathogenicity can be uncoupled from binding in these antibodies.
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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.