Psoriasis is a lifelong, chronic, recurring and highly variable skin disease. Psoriatic plaques are formed through induction of inflammation in the epidermis and deregulation of keratinocyte proliferation and differentiation. This results in red or silvery scaly patches on the surface of the epidermis. To look within the lesions and define the changes in gene expression in psoriasis, investigators compared the transcriptomes of psoriatic plaques, of uninvolved skin of patients and of skin from healthy individuals. In several large studies with many patients, the genes expressed at much higher level in psoriatic plaques included those responsible for the cell cycle, keratinocyte differentiation, and response to wounding; conversely, lipid and fatty acid metabolism enzymes were expressed at reduced levels. The nonlesional and healthy skin appeared fairly similar. The largest study included paired biopsies from 85 individual patients. The same group used transcription profiling to follow the course of treatment in a set of patients, and correlated changes in the transcriptome of blood samples of psoriatic patients. Importantly, a noninvasive technique involving tape-stripping of skin, has been shown effective in transcriptional studies of psoriasis. Current efforts are focused on deconvoluting the contributions of various cell types in psoriasis, keratinocytes, lymphocytes, fibroblasts etc. Taken as a whole, these efforts will lead to personalized medicine, i.e., to specific, individualized treatments of patients with psoriasis.

• Cytokines
• Inflammation
• Metaa nalysis
• Microarrays
• Skinomics