Authors
Tianqi Wei, Xin Huang, Jing Zhu, Guanying Liu, Baiyi Zuo, Zhaokang Zhou, Beilei Xu, Lingling Luo, Chengrang Li
Published in
Inflammation. Jul 15, 2026. Epub Jul 15, 2026.
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+ T cells. Notably, IL32 accelerates depigmentation in the mouse model of vitiligo. These results highlight the therapeutic promise of targeting IL32 to attenuate inflammation and oxidative damage in melanocytes associated with vitiligo.
PMID:
42448875
Bibliographic data and abstract were imported from PubMed on 15 Jul 2026.
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