ArticleClinical and experimental immunology2011
Up-regulation of CCL11 and CCL26 is associated with activated eosinophils in bullous pemphigoid.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 52 citations in OpenAlex.
- The Secretome of Bullous Pemphigoid IgG-Treated Keratinocytes Induces a Pro-Inflammatory Eosinophil Response.Experimental dermatology · 2026Article
- Common Skin Diseases and Metabolic Syndrome: A Proinflammatory Chemokine Perspective.Metabolites · 2026Review
- Article
- Case Report: Dupilumab therapy for immune checkpoint inhibitor-induced bullous pemphigoid enables dual immunotherapy initiation in progressive malignant melanoma.Frontiers in oncology · 2025Article
- Recent advances in the genetics and innate immune cells of bullous pemphigoid.Frontiers in immunology · 2025Review
- Pathophysiology of Bullous Pemphigoid: Role of Type 2 Inflammation and Emerging Treatment Strategies (Narrative Review).Advances in therapy · 2024Review
- Advancements in Bullous Pemphigoid Treatment: A Comprehensive Pipeline Update.American journal of clinical dermatology · 2024Review
- What's New in Cutaneous T-Cell Lymphoma-Associated Pruritus.American journal of clinical dermatology · 2024Review
- 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
- The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets.Frontiers in medicine · 2023Review
- Targeting type 2 inflammation in bullous pemphigoid: current and emerging therapeutic approaches.Frontiers in medicine · 2023Review
- CCL4 Regulates Eosinophil Activation in Eosinophilic Airway Inflammation.International journal of molecular sciences · 2022Article
- A Review of the Immunologic Pathways Involved in Bullous Pemphigoid and Novel Therapeutic Targets.Journal of clinical medicine · 2022Review
- Bullous pemphigoid-What do we know about the most recent therapies?Frontiers in medicine · 2022Review
- Bullous Autoimmune Dermatoses–Clinical Features, Diagnostic Evaluation, and Treatment Options.Deutsches Arzteblatt international · 2021Review
- CCL26 regulates the proportion of CD4Experimental and therapeutic medicine · 2020Article
- Commentary: Proinflammatory role of blister fluid-derived exosomes in bullous pemphigoid.Frontiers in immunology · 2020Article
- Therapeutic Potential of Pharmacological Targeting NLRP3 Inflammasome Complex in Cancer.Frontiers in immunology · 2020Article
- The Intersection of IgE Autoantibodies and Eosinophilia in the Pathogenesis of Bullous Pemphigoid.Frontiers in immunology · 2019Review
- Proteases in Pemphigoid Diseases.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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eosinophils contribute to the pathogenesis of bullous pemphigoid (BP) by secretion of proinflammatory cytokines and proteases. Trafficking of eosinophils into tissue in animal models and asthma depends on interleukin-5 and a family of chemokines named eotaxins, comprising CCL11, CCL24 and CCL26. Up-regulation of CCL11 has been described in BP, but the expression of the other two members of the eotaxin-family, CCL24 and CCL26, has not been investigated. In addition to these chemokines, expression of adhesion molecules associated with eosinophil migration to the skin should be analysed. We demonstrate that similar to CCL11, the concentration of CCL26 was up-regulated in serum and blister fluid of BP patients. In contrast, the concentration of CCL24 was not elevated in sera and blister fluid of the same BP patients. In lesional skin, CCL11 and CCL26 were detected in epidermis and dermis by immunohistochemistry. In contrast to CCL11, CCL26 was expressed strongly by endothelial cells. In line with these findings, eosinophils represented the dominating cell population in BP lesional skin outnumbering other leucocytes. The percentage of eosinophils expressing very late antigen (VLA): VLA-4 (CD49d) and CD11c correlated with their quantity in tissue. Macrophage antigen (MAC)-1 (CD11b/CD18) was expressed constitutively by tissue eosinophils. In conclusion, these data link the up-regulation of the eosinophil chemotactic factor CCL26 in BP to the lesional accumulation of activated eosinophils in the skin. Thereby they broaden the understanding of BP pathogenesis and might indicate new options for therapeutic intervention.
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.