Abstract
Psoriasis is one of the most common human inflammatory skin diseases characterized by hyperproliferation and aberrant differentiation of keratinocytes. Psoriasis is important because it serves as a model for studies of mechanisms of chronic inflammation, and is one of first-choice diseases for proof-of-principle studies of pathogenesis-based therapeutic strategies. In recent years, substantial advances have been made in elucidating the molecular mechanisms of psoriasis. The primary nature of the disease as an epithelial or immunologic disorder, the autoimmune cause of the inflammatory process has been gradually revealed. Critical roles for IFN-alpha secreted by plasmacytoid dendritic cells and the IL-23/Th-17 axis were postulated. This review summarizes recent progress in our understanding of the molecular and immunologic basis of psoriasis and shows how improved insight into disease mechanisms has already resulted in tangible benefits for patients.
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