Obesity and oxidative stress intensify psoriasis through activating IL-17/IL-23 pathway

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.