Scanning the Immunopathogenesis of Psoriasis
AbstractPsoriasis 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. View Full-Text
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Chiricozzi, A.; Romanelli, P.; Volpe, E.; Borsellino, G.; Romanelli, M. Scanning the Immunopathogenesis of Psoriasis. Int. J. Mol. Sci. 2018, 19, 179.
Chiricozzi A, Romanelli P, Volpe E, Borsellino G, Romanelli M. Scanning the Immunopathogenesis of Psoriasis. International Journal of Molecular Sciences. 2018; 19(1):179.Chicago/Turabian Style
Chiricozzi, Andrea; Romanelli, Paolo; Volpe, Elisabetta; Borsellino, Giovanna; Romanelli, Marco. 2018. "Scanning the Immunopathogenesis of Psoriasis." Int. J. Mol. Sci. 19, no. 1: 179.
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