ArticleInflammation2026
Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Oxidative stress-mediated melanocyte injury and subsequent inflammation constitute essential pathogenic mechanisms underlying vitiligo. The secretion of diverse cytokines plays a crucial role in modifying the inflammatory environment characteristics of skin lesions. Interleukin 32 (IL32) is a multifunctional cytokine recognized for its potent pro-inflammatory effects. Here, we observed significantly enhanced IL32 expression in vitiligo skin lesions. The present study investigates the role of IL32 in oxidative stress-driven melanocyte inflammation and its contribution to vitiligo progression by establishing knockdown and overexpression models in PIG cell lines. Our findings demonstrate that oxidative stress triggers IL32 production in melanocytes, and increased IL32 exacerbates oxidative stress-mediated cellular injury. IL32 suppression activates the Nrf2 pathway and mitigates the oxidative stress response. Furthermore, transcriptomic analysis revealed that IL32 may promote the secretion of multiple inflammatory cytokines and chemokines in melanocytes in vitro, especially CXCL9, thereby facilitating the recruitment of CD8
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