ArticleThe American journal of pathology2000
The shed ectodomain of collagen XVII/BP180 is targeted by autoantibodies in different blistering skin diseases.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 186 citations in OpenAlex.
- IgG autoantibodies in bullous pemphigoid induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes.Nature communications · 2025Article
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 2025Review
- Bullous pemphigoid and mucous membrane pemphigoid humoral responses differ in reactivity towards BP180 midportion and BP230.Frontiers in immunology · 2024Article
- Anti-NC16A IgA from Patients with Linear IgA Bullous Dermatosis Induce Neutrophil-Dependent Subepidermal Blistering in Mice.The Journal of investigative dermatology · 2024Article
- Article
- Serological Biomarkers and Their Detection in Autoimmune Bullous Skin Diseases.Dermatology practical & conceptual · 2022Review
- Type XVII collagen: Relevance of distinct epitopes, complement-independent effects, and association with neurological disorders in pemphigoid disorders.Frontiers in immunology · 2022Review
- BP180/Collagen XVII: A Molecular View.International journal of molecular sciences · 2021Review
- Pemphigus-associated cardiomyopathy: report of autoimmune myocarditis and review of literature.ESC heart failure · 2021Review
- Autoantibody Profile of a Cohort of 54 Italian Patients with Linear IgA Bullous Dermatosis: LAD-1 Denoted as a Major Auto-antigen of the Lamina Lucida Subtype.Acta dermato-venereologica · 2020Article
- Collagen XVII Processing and Blistering Skin Diseases.Acta dermato-venereologica · 2020Review
- Autoantibodies Against the Immunodominant Bullous Pemphigoid Epitopes Are Rare in Patients With Dermatitis Herpetiformis and Coeliac Disease.Frontiers in immunology · 2020Article
- Checkpoint Inhibition May Trigger the Rare Variant of Anti-LAD-1 IgG-Positive, Anti-BP180 NC16A IgG-Negative Bullous Pemphigoid.Frontiers in immunology · 2019Article
- Vancomycin Mediates IgA Autoreactivity in Drug-Induced Linear IgA Bullous Dermatosis.The Journal of investigative dermatology · 2018Article
- The Evolving Story of Autoantibodies in Pemphigus Vulgaris: Development of the "Super Compensation Hypothesis".Frontiers in medicine · 2018Review
- Significant Role of Collagen XVII And Integrin β4 in Migration and Invasion of The Less Aggressive Squamous Cell Carcinoma Cells.Scientific reports · 2017Article
- Basement membranes and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Deletion of the major bullous pemphigoid epitope region of collagen XVII induces blistering, autoimmunization, and itching in mice.The Journal of investigative dermatology · 2015Article
- Molecular diagnosis in autoimmune skin blistering conditions.Current molecular medicine · 2014Review
- Bullous pemphigoid IgG induces BP180 internalization via a macropinocytic pathway.The American journal of pathology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen XVII/BP180, an epidermal adhesion molecule, exists as a full-length transmembrane protein and as a soluble 120-kd ectodomain that is shed from the keratinocyte surface by furin-mediated proteolysis. Despite a number of studies on autoantibody targets in blistering skin diseases, it has remained unclear whether the physiologically shed ectodomain of collagen XVII plays a role as an autoantigen. Here we isolated the authentic, soluble form of human collagen XVII and showed that it is an autoantigen recognized by IgG and IgA autoantibodies in different blistering skin diseases and is, in some cases, the preferential target. The ectodomain was isolated from the epidermis, keratinocyte media, amniotic fluid, and pemphigoid blister fluid, and autoantibodies affinity-purified with this ectodomain bound to the proximal surface of the epidermis in normal skin but not in collagen XVII-deficient skin. The antibody reactivity was not dependent on the native conformation or the N-glycosylation of the soluble ectodomain, but was abolished by collagenase treatment. Sera of 81 patients with a clinically active blistering skin disease were reacted with full-length collagen XVII, the authentic soluble ectodomain, and recombinant fragments. In bullous and cicatricial pemphigoid, IgG reactive with full-length collagen XVII also recognized the soluble ectodomain. In linear IgA dermatosis and chronic bullous dermatosis of childhood, IgA targeted the soluble ectodomain more efficiently than the full-length protein. The use of recombinant fragments demonstrated that epitopes were present in several noncollagenous and collagenous subdomains of the molecule, and that a significant portion of the sera targeted Col15 domain, a hitherto unrecognized epitope region.
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