Update on the pathophysiology of psoriasis

Abstract

Psoriasis is a genetically programmed pathologic interaction among skin cells, immunocytes, and numerous biologic signaling molecules that is triggered by environmental stimuli. The immune response is a cellular one; type 1 (TH1) and type 17 (TH17) T cells are activated by IL-12 and IL-23 secreted by antigen-presenting cells (APCs) in the skin. Through various cytokines, such as tumor necrosis factor (TNF) α, these cells cause a chronic inflammatory state and alter epidermal hyperproliferation, differentiation, apoptosis, and neoangiogenesis that produce the cutaneous findings seen in this disease. The newer biologic therapies target the immunologic signaling pathways and cytokines identified in the pathogenesis of psoriasis and provide notable clinical improvement. Further study in the pathogenesis of psoriasis can help identify targets for future therapies.