ArticleThe Journal of investigative dermatology2017
Pro-Inflammatory Chemokines and Cytokines Dominate the Blister Fluid Molecular Signature in Patients with Epidermolysis Bullosa and Affect Leukocyte and Stem Cell Migration.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Tissue and systemic inflammation in dystrophic epidermolysis bullosa: a systematic review and meta-analysis.Orphanet journal of rare diseases · 2025Pooled it
- Impact of low-dose calcipotriol ointment on wound healing, pruritus and pain in patients with dystrophic epidermolysis bullosa: A randomized, double-blind, placebo-controlled trial.Orphanet journal of rare diseases · 2021Trial
- Contribution of HMGB1 to keratinocyte inflammation in recessive dystrophic epidermolysis bullosa.JID innovations : skin science from molecules to population health · 2026Article
- Treatment Landscape for Epidermolysis Bullosa Simplex: A Review of Established and Emerging Therapies.Pediatric dermatology · 2026Review
- Systemic clinical-grade recombinant decorin reduces disease burden and fibrosis in advanced recessive dystrophic epidermolysis bullosa.Molecular therapy. Advances · 2026Article
- An isogenic hiPSC-derived keratinocyte model reveals CXCL10/CXCL11 inflammatory dysregulation in epidermolysis bullosa simplex.Frontiers in cell and developmental biology · 2026Article
- Results of a non-randomized, open-label phase I study evaluating the novel immunomodulatory peptide TCP-25 for treatment of dystrophic epidermolysis bullosa.Orphanet journal of rare diseases · 2025Article
- Cross-sectional analysis of wound-associated soluble factors in early, established, and chronic wounds of recessive dystrophic epidermolysis bullosa patients.Archives of dermatological research · 2025Article
- The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches.JID innovations : skin science from molecules to population health · 2025Review
- Systems immunology integrates the complex endotypes of recessive dystrophic epidermolysis bullosa.Nature communications · 2025Article
- Immunological control of skin development: from homeostasis to developmental pathologies.Frontiers in immunology · 2025Review
- Unveiling the value of C-reactive protein as a severity biomarker and the IL4/IL13 pathway as a therapeutic target in recessive dystrophic epidermolysis bullosa: A multiparametric cross-sectional study.Experimental dermatology · 2024Article
- Article
- Maintenance of chronicity signatures in fibroblasts isolated from recessive dystrophic epidermolysis bullosa chronic wound dressings under culture conditions.Biological research · 2023Article
- Inflammation-mediated fibroblast activation and immune dysregulation in collagen VII-deficient skin.Frontiers in immunology · 2023Article
- T-cell activation and bacterial infection in skin wounds of recessive dystrophic epidermolysis bullosa patients.Experimental dermatology · 2022Article
- Immunological mechanisms underlying progression of chronic wounds in recessive dystrophic epidermolysis bullosa.Experimental dermatology · 2021Review
- Clinical trial of ABCB5+ mesenchymal stem cells for recessive dystrophic epidermolysis bullosa.JCI insight · 2021Article
- Keratins as an Inflammation Trigger Point in Epidermolysis Bullosa Simplex.International journal of molecular sciences · 2021Review
- Deconstructing progressive inflammatory fibrosis in recessive dystrophic epidermolysis bullosa.EMBO molecular medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Hereditary epidermolysis bullosa (EB) is associated with skin blistering and the development of chronic nonhealing wounds. Although clinical studies have shown that cell-based therapies improve wound healing, the recruitment of therapeutic cells to blistering skin and to more advanced skin lesions remains a challenge. Here, we analyzed cytokines and chemokines in blister fluids of patients affected by dystrophic, junctional, and simplex EB. Our analysis revealed high levels of CXCR1, CXCR2, CCR2, and CCR4 ligands, particularly dominant in dystrophic and junctional EB. In vitro migration assays demonstrated the preferential recruitment of CCR4
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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.