Psoriasis vulgaris: an interplay of T lymphocytes, dendritic cells, and inflammatory cytokines in pathogenesis

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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.


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.

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