Abstract
Psoriasis is a chronic inflammatory skin disease with an estimated heritability of 80%. Susceptibility loci identified by genome-wide association studies only account for a small fraction of this heritability. Conversely, gene expression analyses have identified thousands of differentially expressed genes in psoriasis but only a small fraction are likely involved in psoriasis pathophysiology. Of these, IL-17A is highly up-regulated in psoriatic skin and appears to be a driver of disease. In contrast, IL-17D is highly expressed in normal skin but down-regulated in psoriatic plaques.
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