ArticleFrontiers in immunology2018
Specific Inhibition of Complement Activation Significantly Ameliorates Autoimmune Blistering Disease in Mice.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Complement-Activating Capacity of Autoantibodies Correlates With Disease Activity in Bullous Pemphigoid Patients.Frontiers in immunology · 2018Trial
- 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
- Advancements in Bullous Pemphigoid Treatment: A Comprehensive Pipeline Update.American journal of clinical dermatology · 2024Review
- Complement: Functions, location and implications.Immunology · 2023Review
- Extracellular matrix in skin diseases: The road to new therapies.Journal of advanced research · 2023Review
- The neoepitope of the complement C5b-9 Membrane Attack Complex is formed by proximity of adjacent ancillary regions of C9.Communications biology · 2023Article
- The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets.Frontiers in medicine · 2023Review
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Anaphylatoxins spark the flame in early autoimmunity.Frontiers in immunology · 2022Review
- The relevance of complement in pemphigoid diseases: A critical appraisal.Frontiers in immunology · 2022Review
- Bullous pemphigoid-What do we know about the most recent therapies?Frontiers in medicine · 2022Review
- A blistering new era for bullous pemphigoid: A scoping review of current therapies, ongoing clinical trials, and future directions.Annals of medicine and surgery (2012) · 2021Article
- A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy.Antibodies (Basel, Switzerland) · 2021Review
- Characterizing the original anti-C5 function-blocking antibody, BB5.1, for species specificity, mode of action and interactions with C5.Immunology · 2020Article
- Drug Development in Pemphigoid Diseases.Acta dermato-venereologica · 2020Review
- Resolution in bullous pemphigoid.Seminars in immunopathology · 2019Review
- Dual inhibition of complement factor 5 and leukotriene B4 synergistically suppresses murine pemphigoid disease.JCI insight · 2019Article
- Complement Activation in Autoimmune Bullous Dermatoses: A Comprehensive Review.Frontiers in immunology · 2019Review
- Skin Barrier and Autoimmunity-Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Epidermolysis bullosa acquisita (EBA) is an antibody-mediated blistering skin disease associated with tissue-bound and circulating autoantibodies to type VII collagen (COL7). Transfer of antibodies against COL7 into mice results in a subepidermal blistering phenotype, strictly depending on the complement component C5. Further, activation predominantly by the alternative pathway is required to induce experimental EBA, as blistering was delayed and significantly ameliorated only in factor B
Indexed as
Identifiers
What OpenQuestion holds
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.