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- Andrea Chiricozzi
- Dermatology Department, University of Pisa, Via Roma 67, 56126 Pisa, Italy
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- Paolo Romanelli
- Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1295 NW 14th St, Miami, FL 33125, USA
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- Elisabetta Volpe
- The Laboratory of Neuroimmunology, Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy
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- Giovanna Borsellino
- The Laboratory of Neuroimmunology, Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy
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- Marco Romanelli
- Dermatology Department, University of Pisa, Via Roma 67, 56126 Pisa, Italy
説明
<jats:p>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.</jats:p>
収録刊行物
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- International Journal of Molecular Sciences
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International Journal of Molecular Sciences 19 (1), 179-, 2018-01-08
MDPI AG