Interleukin‐17 as a factor linking the pathogenesis of psoriasis with metabolic disorders

Psoriasis is a systemic disease with numerous concomitant metabolic disorders. Apparently, T-helper 17 lymphocytes and interleukin (IL)-17 constitute an important element linking those disorders. The role of IL-17 has been confirmed by numerous studies, although it remains not completely understood, and the study results are controversial. Based on the studies performed so far, it is assumed that IL-17 contributes to development of atherosclerosis by means of: stimulation of production of proinflammatory compounds; induction of apoptosis of endothelial cells and heart muscle cells; stimulation of von Willebrand factor production; and induction of the matrix metalloproteinase-9 (atherosclerotic plaque rupture). On the other hand, IL-17 may exert protective activity due to inhibition of proatherogenic interferon-γ and vascular cell adhesion molecule-1, and production of type I collagen by smooth muscle cells. The role of IL-17 in the pathogenesis of obesity is as important as other proinflammatory cytokines. On the other hand, its deficiency increases diet-induced obesity and accelerates adipose tissue accumulation. Although the role of IL-17A in the pathogenesis of metabolic disorders in humans remains controversial, introduction of anti-IL-17A treatments brings hope that development of metabolic disorders in patients with psoriasis may be inhibited.