ArticleThe Journal of clinical investigation2005
Induction of dermal-epidermal separation in mice by passive transfer of antibodies specific to type VII collagen.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 221 citations in OpenAlex.
- Complement-Activating Capacity of Autoantibodies Correlates With Disease Activity in Bullous Pemphigoid Patients.Frontiers in immunology · 2018Trial
- CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models.Cell communication and signaling : CCS · 2026Article
- Tyrosine kinase signaling pathways as therapeutic targets in autoimmune subepidermal blistering skin diseases (pemphigoid diseases).Frontiers in immunology · 2026Review
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- Therapeutic targeting of alternative pathway and C5 but not C5a protects from disease development in a preclinical model of autoimmune blistering dermatosis.Frontiers in immunology · 2025Article
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- C3 deficiency promotes pulmonary inflammation in AT1R-induced mouse model for systemic sclerosis.Frontiers in immunology · 2024Article
- Epidermolysis Bullosa Acquisita-Current and Emerging Treatments.Journal of clinical medicine · 2023Review
- Luteolin peracetate and gossypolone inhibit immune complex-mediated neutrophil activationFrontiers in immunology · 2023Article
- Monocyte populations are involved in the pathogenesis of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Protocol to Induce Follicular T Helper Cells, Germinal Centers, and Skin Lesions in Mouse Models for Skin Blistering Diseases.Bio-protocol · 2022Article
- Mast cell-deficient miceSkin health and disease · 2022Article
- Risk factors and sequelae of epidermolysis bullosa acquisita: A propensity-matched global study in 1,344 patients.Frontiers in immunology · 2022Article
- Differential expression of C5aR1 and C5aR2 in innate and adaptive immune cells located in early skin lesions of bullous pemphigoid patients.Frontiers in immunology · 2022Article
- The relevance of complement in pemphigoid diseases: A critical appraisal.Frontiers in immunology · 2022Review
- Bullous Autoimmune Dermatoses–Clinical Features, Diagnostic Evaluation, and Treatment Options.Deutsches Arzteblatt international · 2021Review
- A Mitochondrial Polymorphism Alters Immune Cell Metabolism and Protects Mice from Skin Inflammation.International journal of molecular sciences · 2021Article
- Preventive but Not Therapeutic Topical Application of Local Anesthetics Can Inhibit Experimental Epidermolysis Bullosa Acquisita in Mice.Frontiers in immunology · 2021Article
- Topical Application of the PI3Kβ-Selective Small Molecule Inhibitor TGX-221 Is an Effective Treatment Option for Experimental Epidermolysis Bullosa Acquisita.Frontiers in medicine · 2021Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermolysis bullosa acquisita (EBA) is a subepidermal blistering disorder associated with tissue-bound and circulating autoantibodies specific to type VII collagen, a major constituent of the dermal-epidermal junction. Previous attempts to transfer the disease by injection of patient autoantibodies into mice have been unsuccessful. To study the pathogenic relevance of antibodies specific to type VII collagen in vivo, we generated and characterized rabbit antibodies specific to a murine form of this antigen and passively transferred them into adult nude, BALB/c, and C57BL/6 mice. Immune rabbit IgG bound to the lamina densa of murine skin and immunoblotted type VII collagen. Mice injected with purified IgG specific to type VII collagen, in contrast to control mice, developed subepidermal skin blisters, reproducing the human disease at the clinical, histological, electron microscopical, and immunopathological levels. Titers of rabbit IgG in the serum of mice correlated with the extent of the disease. F(ab')(2) fragments of rabbit IgG specific to type VII collagen were not pathogenic. When injected into C5-deficient mice, antibodies specific to type VII collagen failed to induce the disease, whereas C5-sufficient mice were susceptible to blister induction. This animal model for EBA should facilitate further dissection of the pathogenesis of this disease and development of new therapeutic strategies.
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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.