ArticleThe Journal of allergy and clinical immunology2014
Cyclosporine in patients with atopic dermatitis modulates activated inflammatory pathways and reverses epidermal pathology.
Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 papers, 3 of them syntheses that pooled it.
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
60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 178 citations in OpenAlex.
- Biomarkers for therapeutic response and adverse outcomes in atopic dermatitis: A systematic review.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Pooled it
- Immune Tolerance vs. Immune Resistance: The Interaction Between Host and Pathogens in Infectious Diseases.Frontiers in veterinary science · 2022Pooled it
- Meta-analysis derived atopic dermatitis (MADAD) transcriptome defines a robust AD signature highlighting the involvement of atherosclerosis and lipid metabolism pathways.BMC medical genomics · 2015Pooled it
- A phase 2a randomized vehicle-controlled multi-center study of the safety and efficacy of delgocitinib in subjects with moderate-to-severe alopecia areata.Archives of dermatological research · 2023Trial
- Integrated Safety Analysis of Abrocitinib for the Treatment of Moderate-to-Severe Atopic Dermatitis From the Phase II and Phase III Clinical Trial Program.American journal of clinical dermatology · 2021Trial
- Minimally invasive skin tape strip RNA sequencing identifies novel characteristics of the type 2-high atopic dermatitis disease endotype.The Journal of allergy and clinical immunology · 2018Trial
- Major depressive disorder shares systemic immune signatures and potential therapeutic targets with inflammatory skin diseases.Molecular psychiatry · 2026Article
- A Framework for Autonomous AI-Driven Drug Discovery.bioRxiv : the preprint server for biology · 2026Article
- Supporting evidence and recommendations for the management of patients with systemic-eligible atopic dermatitis: A Canadian consensus document.JAAD international · 2026Article
- Dupilumab in Elderly Patients with Atopic Dermatitis-A Systematic Review and Meta-Analysis.Biomedicines · 2026Review
- Article
- Review
- Understanding Atopic Dermatitis: Pathophysiology and Management Strategies.Biomolecules · 2025Review
- Complementary Analysis of Local and Systemic Effects of Dupilumab in Paediatric AD Using Tape Strips and Serum.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- Monoclonal Antibodies: Current Advancements and Future Potential for Atopic Dermatitis Therapy.Current pharmaceutical biotechnology · 2025Review
- The role of chemerin, elafin, and visfatin in the pathogenesis of atopic dermatitis.Frontiers in immunology · 2025Review
- Evaluation of the levels of interleukins IL-4, IL-13, IL-5, IL-10 and IL-33 in atopic dermatitis patients with and without dupilumab therapy.Frontiers in immunology · 2025Article
- IL-4, IL-13, TNF-α and IFN-γ Downregulate CLDN8 Expression Through Activating JAK Signaling Pathway in HaCaT Cells.Clinical, cosmetic and investigational dermatology · 2025Article
- Management of Moderate-to-Severe Atopic Dermatitis in Adults: A Cross-Sectional Survey of Dermatologists Within the Asia-Pacific Region.Dermatology and therapy · 2024Article
- Biologic and Small Molecule Therapy in Atopic Dermatitis.Biomedicines · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundAtopic dermatitis (AD) is the most common inflammatory disease. Evolving disease models link changes in epidermal growth and differentiation to T(H)2/T(H)22 cytokine activation. However, these models have not been tested by in vivo suppression of T-cell cytokines. Cyclosporine (CsA) is an immunosuppressant that is highly effective for severe disease, but its mechanism in AD skin lesions has not been studied.
objectiveWe sought to establish the ability of a systemic immunosuppressant to modulate immune and epidermal alterations that form the pathogenic disease phenotype and to correlate changes with clinical improvement.
methodsCsA's effects on AD skin pathology were evaluated by using gene expression and immunohistochemistry studies in baseline, week 2, and week 12 lesional and nonlesional biopsy specimens from 19 patients treated with 5 mg/kg/d CsA for 12 weeks.
resultsAfter 2 and 12 weeks of treatment, we observed significant reductions of 51% and 72%, respectively, in SCORAD scores. Clinical improvements were associated with significant gene expression changes in lesional but also nonlesional skin, particularly reductions in levels of T(H)2-, T(H)22-, and some T(H)17-related molecules (ie, IL-13, IL-22, CCL17, S100As, and elafin/peptidase inhibitor 3), and modulation of epidermal hyperplasia and differentiation measures.
conclusionsThis is the first study that establishes a relationship between cytokine activation and molecular epidermal alterations, as well as correlations between disease biomarkers in the skin and clinical improvement. The reversal of the molecular phenotype with CsA and the associated biomarkers can serve as a reference for the successful modulation of tissue inflammation with specific immune antagonists in future studies, contributing to the understanding of the specific cytokines involved in epidermal pathology.
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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.