Contribution of the IL-17 Pathway to Psoriasis and Psoriatic Arthritis

被引:0
作者
L. E. Durham
B. W. Kirkham
L. S. Taams
机构
[1] King’s College London,Centre for Molecular and Cellular Biology of Inflammation (CMCBI), Division of Immunology, Infection and Inflammatory Disease
[2] Guy’s and St Thomas’ NHS Trust,Department of Rheumatology
来源
Current Rheumatology Reports | 2015年 / 17卷
关键词
Psoriasis; Psoriatic arthritis; Spondyloarthritis; Interleukin-17; Interleukin-23; Th17 cells; Tc17 cells; IL-17 blockade; Brodalumab; Ixekizumab; Secukinumab; Ustekinumab; CD8+ T Cells; CD4+ T cells;
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摘要
Investigators have accrued compelling evidence that the IL-17 pathway is central to the pathogenesis of psoriasis and psoriatic arthritis. The evidence comprises genome-wide association studies (GWAS), data from experimental murine models and findings from in vitro studies on patients’ cells or tissue biopsies. More recently, the success of drugs blocking the IL-17 pathway in treating both psoriasis (PsO) and psoriatic arthritis (PsA) confirms that IL-17 is a clinically relevant therapeutic target. However, there remain many unanswered questions: is PsA simply an extension of PsO from the skin to the synovial tissue or are there differences in the underlying pathogenesis of these diseases? Which cell type represents the primary source of IL-17 in PsO and PsA? And how are these cells regulated? This review outlines the IL-17 pathway, summarises the evidence supporting its role in PsO and PsA and discusses recent data that may help to address these yet unresolved questions.
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