ABSTRACT

Psoriasis is a chronic inflammatory skin disorder affecting 2-4% of the world’s population. The disease is characterized by epidermal hyperproliferation and inflammation. Psoriasis is considered to be a genetically programmed disease of dysregulated inflammation, which is driven and maintained by multiple components of the immune system. The pathologic collaboration between innate immunity and acquired immunity results in the production of cytokines, chemokines, and growth factors that contribute to the inflammatory infiltrate seen in psoriatic plaques. The aggravated state of innate immunity is represented by the activity of natural killer T cells, dendritic cells, neutrophils and keratinocytes, leading to the recruitment and activation of preferentially type 1 T cells, possibly in an antigen-independent way. The chronic inflammation of psoriasis lesions suggests that this might be due to a deficiency in downregulation processed and/or the persistance of an unknown trigger resulting in an exaggerated innate immune response.