Abstract
In recent years, our knowledge of the immunopathogenesis of chronic inflammatory skin diseases has increased significantly. Accumulating evidence indicates that the complex interaction of structural cells, in particular keratinocytes and endothelial cells, with skin-infiltrating leukocytes is key to our understanding of psoriasis. The recruitment of pathogenic leukocyte subsets into the skin represents a prerequisite for the initiation and maintenance of psoriasis vulgaris and is mediated by a complex chemokine and cytokine network. Results of recent studies associating cytokines and chemokines with a psoriatic phenotype are outlined herein, and their role as therapeutic targets in psoriasis is discussed in detail.
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