MicroRNAs (miRNAs) are ~22 nt noncoding RNAs that can suppress the expression of protein-coding genes by targeting cognate messenger RNAs for translational repression or, less frequently, degradation 
. In the human genome, miRNAs comprise 1-5% of all genes making them the most abundant class of regulators. The high sequence conservation of many miRNAs among distantly related organisms suggests strong evolutionary pressure and participation in essential processes 
. Indeed, miRNAs have regulatory roles in development, differentiation, organogenesis, stem cell and germline proliferation, growth control and apoptosis. Moreover, deregulation of miRNA expression may contribute to human diseases; in particular, miRNAs are often aberrantly expressed or mutated in cancer 
. Thus, miRNAs represent important targets for potential therapeutic and diagnostic agents 
While miRNAs are known to regulate cell growth, apoptosis, differentiation and morphological development, neither their expression nor roles have been characterized in skin diseases. Psoriasis is the most prevalent chronic inflammatory skin disease in adults affecting 1-3% of the population worldwide with a substantial negative impact on the patients' quality of life 
. A complex interplay of genetic and environmental factors together with immunoregulatory abnormalities is thought to play a critical role in the pathogenesis of this disease. Keratinocytes and infiltrating immune cells play a cooperative role in the formation of psoriasis lesions; however, the exact molecular mechanisms regulating the complex interactions among resident skin cells and infiltrating immune cells are still not completely understood. Investigations analyzing the molecular background of psoriasis have identified hundreds of disease-associated genes and proteins with aberrant expression 
, however, our understanding about the regulatory networks underlying the altered expression of these genes is far from being complete.
Here, we demonstrate that psoriasis is characterized by a specific miRNA expression profile that differs from that of healthy skin or another chronic inflammatory disease, atopic eczema. Among the miRNAs overexpressed in psoriasis, we identified a keratinocyte-specific miRNA (miR-203) and a leukocyte-derived miRNA (miR-146a). The up-regulation of miR-203 in psoriatic plaques was concurrent with the down-regulation of an evolutionary conserved target of miR-203, suppressor of cytokine signaling 3 (SOCS-3), which is involved in inflammatory responses and keratinocyte functions. These results suggest that miRNAs contribute to psoriasis pathogenesis by modulating protein expression and cellular functions in both keratinocytes and infiltrating immune cells. Thus, our findings reveal a new layer of regulatory mechanisms in the pathogenesis of chronic inflammatory skin diseases.