Psoriasis vulgaris: cutaneous lymphoid tissue supports T-cell activation and 'type 1' inflammatory gene expression

Psoriasis vulgaris is a common inflammatory skin disease that involves infiltration of leukocytes, activation of skin-resident cells and increased production of numerous cytokines, chemokines and inflammatory molecules. This Review presents an integrated view of disease pathogenesis, taking into account immune biology, broad-scale genomic characterization and the response of psoriasis to immune-targeted therapies. Recent studies suggest that activated dendritic cells (DCs) and T cells are central to its pathogenesis, causing 'inflammation' through a pathway of sequential interleukin-23 (IL-23) synthesis, interferon-gamma (IFN-gamma) production, activation of STAT1 (signal transducer and activator of transcription 1) and subsequent transcription of a broad series of IFN- and STAT-1-regulated genes. In situ expression of macrophage inflammatory protein-3beta (MIP-3beta; CCL19), secondary lymphoid tissue chemokine (SLC; CCL21) and other chemokines normally confined to formal lymphoid tissues, might help to sustain DC accumulation and overall activation of this inflammatory pathway.