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Vitiligo is characterized by underlying immunometabolism mechanisms. These serve as the basis for understanding the pathogenic mechanisms and the development of novel therapeutic approaches.

Vitiligo is an autoimmune depigmenting skin disorder associated with selective melanocyte loss. The pathogenesis of vitiligo comprises biological, environmental, autoimmune, and genetic factors; however, complete molecular mechanisms underlying the development of vitiligo are yet to be known. This review, published in the Frontiers in Immunology, discusses the immunometabolism reprogramming in vitiligo and the newer treatment options for this autoimmune disorder.

The pathogenic mechanisms implicated in vitiligo include abnormal glucose metabolism, lipid metabolism, and oxidative stress. Vitiligo patients are at a significantly higher risk for diabetes and have higher levels of fasting glucose. Pro-inflammatory and certain anti-inflammatory cytokines are elevated among individuals with active vitiligo. This leads to the development of insulin resistance and other metabolic abnormalities. Vitiligo is also associated with dyslipidemia, manifested by metabolic abnormalities such as higher cholesterol, leptin, low-density lipoprotein (LDL), and triglyceride (TG) levels. Abnormal lipid metabolism in vitiligo patients may give rise to T cell dysfunction.

Regarding oxidative stress in vitiligo, altered antioxidant systems are involved in the pathogenesis of the disease. Vitiligo patients have low levels of superoxide dismutase (SOD), catalase (CAT), glucose-6-phosphate dehydrogenase (G6PD), and glutathione peroxidase (GPx). This leads to melanocyte senescence and the removal of these melanocytes by the immune cells. Chronic oxidative stress (OS) in vitiligo results in an increased accumulation of reactive oxygen species (ROS). Impaired redox homeostasis is attributed to mitochondrial dysfunction. Prolonged endoplasmic reticulum (ER) stress is associated with the activation and secretion of pro-inflammatory cytokines, promoting further ER and oxidative stress. Regarding the novel therapeutic strategies for immunometabolism in vitiligo, the JAK-STAT pathway, nuclear factor-like factor 2 (Nrf2)–antioxidant response element (ARE) pathway, and IFN-Ɣ chemokine axis serve as therapeutic targets.

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In summary, immunometabolism mechanisms in vitiligo have emerged as an effective basis for understanding the disease pathogenesis and serving as novel therapeutic targets. Further research studies may evaluate the therapeutic safety and efficacy of these novel immunometabolism approaches in treating vitiligo.

Reference

Lyu, C., & Sun, Y. (2022). Immunometabolism in the pathogenesis of vitiligo. Front Immunol, 13, 1055958. https://doi.org/10.3389/fimmu.2022.1055958