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Obesity and oxidative stress intensify psoriasis through activating IL-17/IL-23 pathway
Suci Vikasari , Elin Sukandar , Tri Suciati , I Ketut Adnyana
Abstract:   (348 Views)
Psoriasis is an autoimmune disease characterized by keratinocyte hyperproliferation and thickness in the skin. 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 signalling via cytokines interleukin-17A (IL-17A), IL-17, IL-23, tumor necrosis factor alfa (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 IL-17/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.
 
Keywords: Psoriasis, Autoimmune, Obese, Oxidative stress, IL-17/IL-23 pathway
     
Types of Manuscript: Mini-review | Subject: Blood and Immune System
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