ArticleArchives of dermatological research1996
Detection of elevated levels of IL-4, IL-6, and IL-10 in blister fluid of bullous pemphigoid.
Article in Archives of dermatological research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 90 citations in OpenAlex.
- Shared Mechanistic Pathways in Bullous Pemphigoid, Chronic Spontaneous Urticaria, Prurigo Nodularis, and Chronic Prurigo of Unknown Origin: Implications for Targeted Therapies.American journal of clinical dermatology · 2026Review
- JAK-STAT pathway, type I/II cytokines, and new potential therapeutic strategy for autoimmune bullous diseases: update on pemphigus vulgaris and bullous pemphigoid.Frontiers in immunology · 2025Review
- Pruritogens in pemphigoid diseases: Possible therapeutic targets for a burdensome symptom.The Journal of dermatology · 2023Review
- Targeting type 2 inflammation in bullous pemphigoid: current and emerging therapeutic approaches.Frontiers in medicine · 2023Review
- Computer-aided classification of indirect immunofluorescence patterns on esophagus and split skin for the detection of autoimmune dermatoses.Frontiers in immunology · 2023Article
- The Role of Interleukins in the Pathogenesis of Dermatological Immune-Mediated Diseases.Advances in therapy · 2022Review
- Innate immune activation as cofactor in pemphigus disease manifestation.Frontiers in immunology · 2022Article
- Bullous pemphigoid-What do we know about the most recent therapies?Frontiers in medicine · 2022Review
- Type XVII collagen: Relevance of distinct epitopes, complement-independent effects, and association with neurological disorders in pemphigoid disorders.Frontiers in immunology · 2022Review
- IL-13 Genetic Susceptibility to Bullous Pemphigoid: A Potential Target for Treatment and a Prognostic Marker.Frontiers in immunology · 2022Observational
- Signal Integration by Translocation and Phosphorylation of PKCδ in the B Cell Alternate Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Immunomodulator Galectin-9 is Increased in Blood and Skin of Patients with Bullous Pemphigoid.Acta dermato-venereologica · 2021Article
- Resolution in bullous pemphigoid.Seminars in immunopathology · 2019Review
- Blister Fluid Induces MMP-9-Associated M2-Type Macrophages in Bullous Pemphigoid.Frontiers in immunology · 2019Article
- The Intersection of IgE Autoantibodies and Eosinophilia in the Pathogenesis of Bullous Pemphigoid.Frontiers in immunology · 2019Review
- Tyrosine Kinases in Autoimmune and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Expression of the JAK/STAT Signaling Pathway in Bullous Pemphigoid and Dermatitis Herpetiformis.Mediators of inflammation · 2017Article
- A network map of Interleukin-10 signaling pathway.Journal of cell communication and signaling · 2016Article
- Hsp90 blockade modulates bullous pemphigoid IgG-induced IL-8 production by keratinocytes.Cell stress & chaperones · 2014Article
- Collagen XVII (BP180) modulates keratinocyte expression of the proinflammatory chemokine, IL-8.Experimental dermatology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease with autoantibodies directed against antigens associated with hemidesmosomes of basal keratinocytes. In addition to autoantibodies and activated complement, cellular mechanisms are crucial for blister formation in this disease. Mononuclear cells, which are the first cells infiltrating BP lesions, mainly belong to CD3, CD4+ T-helper (Th) cells. Elevated concentrations of IL-2, IFN gamma, TNF beta, and IL-5 have been recently demonstrated in BP blister fluid. In this study, we were interested in levels of other Th-type cytokines, including IL-3, IL-4, IL-6, IL-10, and GM-CSF in blister fluid of BP. Cytokines were determined by ELISA or bioassay. Levels in the blister fluid from ten BP patients were compared with those in serum samples taken at the time of blister puncture and with those in suction blister fluid of ten healthy volunteers. In blister fluid of BP, we found significantly elevated concentrations of IL-4, IL-6, and IL-10 relative to both concurrent serum samples and suction blister fluid from controls. No differences were detected for either IL-3 or GM-CSF. Our results suggest that IL-4, IL-6, and IL-10 are released at the site of blister formation in 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.