BackgroundChronic spontaneous urticaria (CSU) is considered an autoimmune disorder in 50% of cases at least, in which T‐ and mast cell mediators are considered to be the primary cause of symptoms. However, H1‐antihistamines, cyclosporine A, and omalizumab fail to achieve complete symptom amelioration in up to 70% of patients. This suggests that other inflammatory pathways are involved and that additional and more effective treatments need to be developed.ObjectiveThis preliminary report examines the possibility that interleukin‐17 (IL‐17), a cytokine involved in the pathogenesis of many autoimmune diseases, may contribute to CSU and its inhibition may offer a relevant therapeutic target.MethodsThe expression of IL‐17A in skin biopsies of 20 CSU patients and 10 healthy controls was determined by quantitative histomorphometry. We also assessed the response to secukinumab (anti‐IL‐17A) treatment patients of eight severe CSU (7‐day urticaria activity score UAS7 32‐40) who were H1‐antihistamine and omalizumab‐resistant.ResultsIncreased numbers of CD4+ T cells and mast cells were present in both lesional and non‐lesional skin of CSU patients compared with healthy controls. Both types of cells were strongly positive for IL‐17A and found to be in close proximity to each other. All eight patients treated with the anti‐IL‐17A antibody, secukinumab, showed significant improvement in CSU disease activity. The action of secukinumab was shown to be relatively slow in onset. The significant reduction in disease activity from baseline UAS7 was demonstrated to be 55% and 82% at 30 and 90 days, respectively.ConclusionsThese findings suggest that IL‐17 is involved in the pathogenesis of CSU and that IL‐17 should be investigated as a therapeutic target in future studies with larger numbers of patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.