ArticleThe Journal of clinical investigation2001
Mast cells play a key role in neutrophil recruitment in experimental bullous pemphigoid.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 229 citations in OpenAlex.
- Autoimmune Bullous Diseases: Therapeutic Update.Drugs · 2026Review
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 2025Review
- Pathophysiology of Bullous Pemphigoid: Role of Type 2 Inflammation and Emerging Treatment Strategies (Narrative Review).Advances in therapy · 2024Review
- Treatment of Bullous Pemphigoid with Avdoralimab: Multicenter, Randomized, Open-Labeled Phase 2 Study.JID innovations : skin science from molecules to population health · 2024Article
- Anti-NC16A IgA from Patients with Linear IgA Bullous Dermatosis Induce Neutrophil-Dependent Subepidermal Blistering in Mice.The Journal of investigative dermatology · 2024Article
- Eosinophils, Basophils, and Neutrophils in Bullous Pemphigoid.Biomolecules · 2023Review
- IL-33-mediated activation of mast cells is involved in the progression of imiquimod-induced psoriasis-like dermatitis.Cell communication and signaling : CCS · 2023Article
- The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets.Frontiers in medicine · 2023Review
- Immunology of amyotrophic lateral sclerosis - role of the innate and adaptive immunity.Frontiers in neuroscience · 2023Review
- Targeting type 2 inflammation in bullous pemphigoid: current and emerging therapeutic approaches.Frontiers in medicine · 2023Review
- Adaptive and innate immune pathogenesis of bullous pemphigoid: A review.Frontiers in immunology · 2023Review
- Altered early immune response after fracture and traumatic brain injury.Frontiers in immunology · 2023Article
- Mechanism of Fuzheng Kang'ai Formula Regulating Tumor Microenvironment in Non-Small Cell Lung Cancer.Chinese journal of integrative medicine · 2022Article
- Mast cell-deficient miceSkin health and disease · 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
- Insights Into the Pathogenesis of Bullous Pemphigoid: The Role of Complement-Independent Mechanisms.Frontiers in immunology · 2022Review
- May Bacterial Infections Trigger Bullous Pemphigoid? Case Report and Review of Literature.Microorganisms · 2021Article
- Granzyme B inhibition reduces disease severity in autoimmune blistering diseases.Nature communications · 2021Article
- Preventive but Not Therapeutic Topical Application of Local Anesthetics Can Inhibit Experimental Epidermolysis Bullosa Acquisita in Mice.Frontiers in immunology · 2021Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Bullous pemphigoid (BP) is an inflammatory subepidermal blistering disease associated with an IgG autoimmune response to the hemidesmosomal protein BP180. Passive transfer of antibodies to the murine BP180 (mBP180) ectodomain triggers a blistering skin disease in mice that depends on complement activation and neutrophil infiltration and closely mimics human BP. In the present study, we show that mast cells (MCs) play a crucial role in experimental BP. Wild-type mice injected intradermally with pathogenic anti-mBP180 IgG exhibited extensive MC degranulation in skin, which preceded neutrophil infiltration and subsequent subepidermal blistering. In contrast, mice genetically deficient in MCs or MC-sufficient mice pretreated with an inhibitor of MC degranulation failed to develop BP. Further, MC-deficient mice reconstituted in skin with MCs became susceptible to experimental BP. Despite the activation of complement to yield C3a and C5a, in the absence of MCs, accumulation of neutrophils at the injection site was blunted. The lack of response due to MC deficiency was overcome by intradermal administration of a neutrophil chemoattractant, IL-8, or by reconstitution of the injection sites with neutrophils. These findings provide the first direct evidence to our knowledge that MCs play an essential role in neutrophil recruitment during subepidermal blister formation in experimental BP.
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.