Purpose of review: Discuss and update concepts and hypotheses for the pathogenesis of psoriasis based on new research reports (primarily from 2003 and early 2004).
Recent findings: Increases in newly defined dendritic cell subsets, cytokines, and chemokines have been identified in psoriasis lesions and have modified views of T-cell-mediated pathogenesis. In addition, the psoriasis transcriptome has been defined by large-scale genomic expression studies, and these data suggest distinct molecular mechanisms of type 1 T-cell-mediated inflammation. Somewhat surprisingly, therapeutic clinical trials suggest that tumor necrosis factor is a major pathogenic cytokine in psoriasis, whereas translational studies point to roles of other innate pathways mediated by heat shock proteins, glycolipids, natural killer T cells, or dendritic cells in disease pathogenesis.
Summary: An interactive network of inflammatory cytokines, chemokines, dendritic cells, and type 1 T cells or natural killer T cells potentially drives pathogenic inflammation in psoriasis vulgaris. Continued clinical studies with defined immune antagonists provide a critical means to dissect the contribution of different cell subsets and genomic pathways to the pathogenesis of psoriasis vulgaris.