ArticleMolecular medicine (Cambridge, Mass.)2017
Reduced skin blistering in experimental epidermolysis bullosa acquisita after anti-TNF treatment.
Article in Molecular medicine (Cambridge, Mass.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Pemphigoid disease model systems for clinical translation.Frontiers in immunology · 2025Review
- Paradoxical and bimodal immune-mediated dermatological side effects of TNF-α inhibitors: A comprehensive review.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Review
- Inhibition of interferon gamma impairs induction of experimental epidermolysis bullosa acquisita.Frontiers in immunology · 2024Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Case Report: Biological treatment of epidermolysis bullosa acquisita: report on four cases and literature review.Frontiers in immunology · 2023Review
- There Is Strength in Numbers: Quantitation of Fc Gamma Receptors on Murine Tissue-Resident Macrophages.International journal of molecular sciences · 2021Article
- Immunomodulator Galectin-9 is Increased in Blood and Skin of Patients with Bullous Pemphigoid.Acta dermato-venereologica · 2021Article
- Editorial: Skin Autoimmunity.Frontiers in immunology · 2021Article
- Skin Barrier and Autoimmunity-Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin.Frontiers in immunology · 2019Review
- Therapeutic Effect of a Novel Phosphatidylinositol-3-Kinase δ Inhibitor in Experimental Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2018Article
- Whole-Genome Expression Profiling in Skin Reveals SYK As a Key Regulator of Inflammation in Experimental Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2018Article
- Epidermolysis Bullosa Acquisita: The 2019 Update.Frontiers in medicine · 2018Review
- The Immunometabolomic Interface Receptor Hydroxycarboxylic Acid Receptor 2 Mediates the Therapeutic Effects of Dimethyl Fumarate in Autoantibody-Induced Skin Inflammation.Frontiers in immunology · 2018Article
- Regulatory T Cells Suppress Inflammation and Blistering in Pemphigoid Diseases.Frontiers in immunology · 2017Article
- Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017Review
- Role of immune cells in the ocular manifestations of pemphigoid diseases.Therapeutic advances in ophthalmologyReview
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermolysis bullosa acquisita (EBA) is a difficult-to-treat subepidermal autoimmune blistering skin disease (AIBD) with circulating and tissue-bound anti-type VII collagen antibodies. Different reports have indicated an increased concentration of tumor necrosis factor alpha (TNF) in the serum and blister fluid of patients with subepidermal AIBDs. Furthermore, successful anti-TNF treatment has been reported for individual patients with AIBDs. Here, we show that in mice, induction of experimental EBA by repeated injections of rabbit-anti mouse type VII collagen antibodies led to increased expression of TNF in skin, as determined by real-time PCR and immunohistochemistry. To investigate if the increased TNF expression is of functional relevance in experimental EBA, we inhibited TNF function using the soluble TNF receptor fusion protein etanercept (Enbrel®) or a monoclonal antibody to murine TNF. Interestingly, mice receiving either of these two treatments showed significantly milder disease progression than controls. In addition, immunohistochemical staining demonstrated reduced numbers of macrophages in lesional skin in mice treated with TNF inhibitors compared to controls. Furthermore, etanercept treatment significantly reduced the disease progression in immunization-induced EBA. In conclusion, the increased expression of TNF in experimental EBA is of functional relevance, as both the prophylactic blockade of TNF and the therapeutic use of etanercept impaired the induction and progression of experimental EBA. Thus, TNF is likely to serve as a new therapeutic target for EBA and AIBDs with a similar pathogenesis.
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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.