Trial reportThe Journal of allergy and clinical immunology2012
IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis.
Trial report in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 7 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
162 citing papers in PubMed, 7 syntheses or guidelines pooled it, 372 citations in OpenAlex.
- Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis.The Cochrane database of systematic reviews · 2022Pooled it
- Association between IL-17A, IL-17F and IL-17RA gene polymorphisms and susceptibility to psoriasis and psoriatic arthritis: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Pooled it
- Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis.The Cochrane database of systematic reviews · 2021Pooled it
- Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis.The Cochrane database of systematic reviews · 2020Pooled it
- Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis.The Cochrane database of systematic reviews · 2017Pooled 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
- Meta-analysis derived (MAD) transcriptome of psoriasis defines the "core" pathogenesis of disease.PloS one · 2012Pooled it
- Efficacy of Ixekizumab in Chinese Patients with Moderate-to-Severe Psoriasis and Special Body Area Involvement: Sub-analysis of a Randomized, Double-Blind, Multicenter Phase 3 Study.Advances in therapy · 2025Trial
- Evaluation of Ixekizumab Treatment for Patients With Pityriasis Rubra Pilaris: A Single-Arm Trial.JAMA dermatology · 2020Trial
- Assessment of serum biomarkers in patients with plaque psoriasis on secukinumab.The Journal of dermatology · 2020Trial
- Assessment and Clinical Relevance of Serum IL-19 Levels in Psoriasis and Atopic Dermatitis Using a Sensitive and Specific Novel Immunoassay.Scientific reports · 2019Trial
- An airway epithelial IL-17A response signature identifies a steroid-unresponsive COPD patient subgroup.The Journal of clinical investigation · 2019Trial
- Clinical efficacy and IL-17 targeting mechanism of Indigo naturalis as a topical agent in moderate psoriasis.BMC complementary and alternative medicine · 2017Trial
- Gene Expression and Pharmacodynamic Changes in 1,760 Systemic Lupus Erythematosus Patients From Two Phase III Trials of BAFF Blockade With Tabalumab.Arthritis & rheumatology (Hoboken, N.J.) · 2017Trial
- Evidence that a neutrophil-keratinocyte crosstalk is an early target of IL-17A inhibition in psoriasis.Experimental dermatology · 2015Trial
- Trial
- Modulation of epidermal transcription circuits in psoriasis: new links between inflammation and hyperproliferation.PloS one · 2013Trial
- Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PRELP negatively regulates IL-17A-mediated proliferation and the inflammatory response in psoriasis.Signal transduction and targeted therapy · 2026Article
- TYMP upregulation mediated by the hyperactivated IL-17/NF-κB1 axis promotes psoriasis through enhancing aberrant keratinization and neutrophil-mediated inflammation.Biology direct · 2026Article
102 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIn subjects with psoriasis, inflammation and epidermal hyperplasia are thought to be controlled by T cell-derived cytokines. Evidence suggests that the T(H)17 cell cytokine IL-17A (IL-17) might play a role in disease pathogenesis.
objectiveWe sought to understand the effect that neutralization of IL-17 has on the clinical features of psoriasis and to understand the role that IL-17 has in inflammatory pathways underlying psoriasis in human subjects.
methodsWe examined skin lesions obtained from 40 subjects participating in a phase I, randomized, double-blind, placebo-controlled trial of the anti-IL-17 mAb ixekizumab (previously LY2439821) in which subjects received 5, 15, 50, or 150 mg of subcutaneous ixekizumab or placebo at weeks 0, 2, and 4.
resultsThere were significant dose-dependent reductions from baseline in keratinocyte proliferation, hyperplasia, epidermal thickness, infiltration into the dermis and epidermis by T cells and dendritic cells, and keratinocyte expression of innate defense peptides at 2 weeks. By week 6, the skin appeared normal. Quantitative RT-PCR and microarrays revealed an ablation of the disease-defining mRNA expression profile by 2 weeks after the first dose of study drug. The effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α was of higher magnitude at 2 weeks than in prior studies with TNF-α antagonism.
conclusionOur data suggest that IL-17 is a key "driver" cytokine that activates pathogenic inflammation in subjects with psoriasis. Neutralizing IL-17 with ixekizumab might be a successful therapeutic strategy in psoriasis.
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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.