ArticleThe Journal of clinical investigation1994
92-kD gelatinase is produced by eosinophils at the site of blister formation in bullous pemphigoid and cleaves the extracellular domain of recombinant 180-kD bullous pemphigoid autoantigen.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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.
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
59 citing papers in PubMed, 217 citations in OpenAlex.
- Tissue Levels of MMP-9 and Granzyme B in Patients With Bullous Pemphigoid: A Case-Control Study.International journal of dermatology · 2026Article
- The Secretome of Bullous Pemphigoid IgG-Treated Keratinocytes Induces a Pro-Inflammatory Eosinophil Response.Experimental dermatology · 2026Article
- Hemidesmosome Mutations Contribute to the Onset and Severity of Acquired Autoimmune Bullous Diseases.MedComm · 2026Article
- The role of matrix metalloproteinase 9 in immune-mediated skin diseases.Frontiers in immunology · 2026Review
- Mendelian Randomization and Experimental Validation Identify Key Immune Signatures in Bullous Pemphigoid.Clinical, cosmetic and investigational dermatology · 2026Article
- Matrix Metalloproteinases in Inflammatory Dermatoses.International journal of molecular sciences · 2025Review
- Systemic Implications of Bullous Pemphigoid: Bridging Dermatology and Internal Medicine.Diagnostics (Basel, Switzerland) · 2024Review
- Co-Treatment with Phlorotannin and Extracellular Vesicles fromAntioxidants (Basel, Switzerland) · 2024Article
- Advancing Treatment in Bullous Pemphigoid: A Comprehensive Review of Novel Therapeutic Targets and Approaches.Clinical reviews in allergy & immunology · 2023Review
- The Eotaxin-1/CCR3 Axis and Matrix Metalloproteinase-9 Are Critical in Anti-NC16A IgE-Induced Bullous Pemphigoid.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Eosinophils, Basophils, and Neutrophils in Bullous Pemphigoid.Biomolecules · 2023Review
- Bullous pemphigoid: The role of type 2 inflammation in its pathogenesis and the prospect of targeted therapy.Frontiers in immunology · 2023Review
- Targeting type 2 inflammation in bullous pemphigoid: current and emerging therapeutic approaches.Frontiers in medicine · 2023Review
- Insights Into the Pathogenesis of Bullous Pemphigoid: The Role of Complement-Independent Mechanisms.Frontiers in immunology · 2022Review
- Targeting the stem cell niche: role of collagen XVII in skin aging and wound repair.Theranostics · 2022Review
- IL-13 Genetic Susceptibility to Bullous Pemphigoid: A Potential Target for Treatment and a Prognostic Marker.Frontiers in immunology · 2022Observational
- Successful induction treatment of bullous pemphigoid using reslizumab: a case report.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
- EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis.The Journal of cell biology · 2021Article
- A Scoping Review of the Role of Metalloproteinases in the Pathogenesis of Autoimmune Pemphigus and Pemphigoid.Biomolecules · 2021Article
- IgE autoantibodies in serum and skin of non-bullous and bullous pemphigoid patients.Journal of the European Academy of Dermatology and Venereology : JEADV · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Eosinophils are prominent in bullous pemphigoid (BP), and proteases secreted from these and other inflammatory cells may induce disruption of the basement membrane. We used in situ hybridization and immunohistochemistry to localize the sites of 92-kD gelatinase expression in BP lesions. In all samples (20/20), a strong signal for gelatinase mRNA was detected only in eosinophils and was most pronounced where these cells accumulated at the floor of forming blisters. No other cells were positive for enzyme mRNA. Both eosinophils and neutrophils, however, contained immunoreactive 92-kD gelatinase indicating that active expression occurred only in eosinophils. Degranulated eosinophils were also seen near blisters, and as demonstrated by gelatin zymography, immunoblotting, and ELISA, 92-kD gelatinase protein was prominent in BP blister fluid. No other gelatinolytic activity was specifically detected in BP fluid, and only small amounts of 92-kD gelatinase were present in suction blister fluids. As demonstrated in vitro, 92-kD gelatinase cleaved the extracellular, collagenous domain of recombinant 180-kD BP autoantigen (BP180, BPAG2, HD4, type XVII collagen), a transmembrane molecule of the epidermal hemidesmosome. Our results suggest that production and release 92-kD gelatinase by eosinophils contributes significantly to tissue damage in BP.
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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.