Scanning the Immunopathogenesis of Psoriasis

Author： Chiricozzi Andrea Romanelli Paolo Volpe Elisabetta Borsellino Giovanna Romanelli Marco

Publisher： MDPI

E-ISSN： 1422-0067|19|1|179-179

ISSN： 1422-0067

Source： International Journal of Molecular Sciences, Vol.19, Iss.1, 2018-01, pp. : 179-179

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Abstract

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)-α, IL-23, IL-22, interferon (IFN)-α, and IFN-γ 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.