The Pathophysiology of Psoriasis

Abstract

Psoriasis is a genetically programmed pathologic interaction between skin cells, immunocytes, and numerous biologic signaling molecules triggered by environmental stimuli. The immune response is a cellular one; TH1 and TH17 cells are activated by IL-12 and IL-23 secreted by antigen presenting cells in the skin. Through various cytokines such as TNF alpha these cells cause a chronic inflammatory state and alter epidermal hyperproliferation, differentiation, apoptosis, and neoangiogenesis that produce the findings seen in this disease. The newer biologic therapies target the immunologic signaling pathways and cytokines identified in the pathogenesis of psoriasis and have proved to provide significant clinical improvement. Further study in the pathogenesis of psoriasis can help identify targets for future therapies.