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Interleukin‐17 as a factor linking the pathogenesis of psoriasis with metabolic disorders
Author(s) -
OwczarczykSaczonek Agnieszka,
Placek Waldemar
Publication year - 2017
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.13420
Subject(s) - proinflammatory cytokine , medicine , pathogenesis , psoriasis , interleukin , immunology , metabolic syndrome , cell adhesion molecule , endocrinology , inflammation , cytokine , diabetes mellitus
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.