Volume 28, Issue 1 (March 2024)                   Physiol Pharmacol 2024, 28(1): 18-26 | Back to browse issues page

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Vikasari S, Sukandar E, Suciati T, Adnyana I K. Obesity and oxidative stress intensify psoriasis through activating IL-17/IL-23 pathway. Physiol Pharmacol 2024; 28 (1) : 4
URL: http://ppj.phypha.ir/article-1-1969-en.html
Obesity and oxidative stress intensify psoriasis through activating IL-17/IL-23 pathway
Suci Vikasari , Elin Sukandar , Tri Suciati , I Ketut Adnyana
Abstract:   (1423 Views)
Psoriasis is an autoimmune disease characterized by keratinocyte hyperproliferation and skin thickening. Psoriasis is caused by a complicated interaction between the innate and acquired immune systems. In the skin, this reaction produces abnormal T helper cell (Th1, Th17, and Th23) reactivation. Keratinocyte hyperproliferation is caused by increased cell signaling via cytokines interleukin-17A (IL-17A), IL-17, IL-23, tumor necrosis factor alpha (TNF-α), and interferon-gamma (INF-γ). Obesity, free fatty acids, microorganisms in the skin and digestive tract, free radicals in the body, and the cardiovascular system are also essential variables in psoriasis. Several variables influence the cytokine activation of the IL17/IL-23 pathway. Obesity, which is marked by changes in lipid profile in psoriasis patients, is linked to increased oxidative stress and the generation of proinflammatory cytokines, both of which can potentially trigger psoriasis relapse. Antioxidant-rich diet and intake can be employed as one of the stages in preventing psoriasis recurrence.
Article number: 4
Keywords: Psoriasis, Autoimmune, Obese, Oxidative stress, IL-17/IL-23 pathway
Full-Text [PDF 875 kb]   (161 Downloads)    
Type of Manuscript: Mini-review | Subject: Blood and Immune System
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