期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 19, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms19010179
关键词
psoriasis; pathogenesis; immunology; autoantigen; IL-17; IL-23; cytokines; chemokines; autoreactive T cells; dendritic cells
Psoriasis is a chronic inflammatory skin disease, the immunologic model of which has been profoundly revised following recent advances in the understanding of its pathophysiology. In the current model, a crosstalk between keratinocytes, neutrophils, mast cells, T cells, and dendritic cells is thought to create inflammatory and pro-proliferative circuits mediated by chemokines and cytokines. Various triggers, including recently identified autoantigens, Toll-like receptor agonists, chemerin, and thymic stromal lymphopoietin may activate the pathogenic cascade resulting in enhanced production of pro-inflammatory and proliferation-inducing mediators such as interleukin (IL)-17, tumor necrosis factor (TNF)-, IL-23, IL-22, interferon (IFN)-, and IFN- by immune cells. Among these key cytokines lie therapeutic targets for currently approved antipsoriatic therapies. This review aims to provide a comprehensive overview on the immune-mediated mechanisms characterizing the current pathogenic model of psoriasis.
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