白细胞介素32通过促进炎症和氧化应激诱导的黑素细胞损伤加重白癜风
Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.
摘要(中文译文)
氧化应激介导的黑素细胞损伤及随后的炎症反应是白癜风发病的基本病理机制。多种细胞因子的分泌在改变皮损炎症环境特征中发挥关键作用。白细胞介素32（IL32）是一种多功能细胞因子，以其强效促炎作用而著称。本研究中，我们观察到白癜风皮损中IL32表达显著增强。本研究通过在PIG细胞系中建立敲低和过表达模型，探讨IL32在氧化应激驱动的黑素细胞炎症中的作用及其对白癜风进展的贡献。我们的研究结果表明，氧化应激触发黑素细胞产生IL32，而IL32增加会加剧氧化应激介导的细胞损伤。抑制IL32可激活Nrf2通路并减轻氧化应激反应。此外，转录组分析揭示，IL32可能在体外促进黑素细胞分泌多种炎症细胞因子和趋化因子，尤其是CXCL9，从而促进CD8 T细胞的募集。值得注意的是，IL32加速了白癜风小鼠模型的脱色素进程。这些结果凸显了靶向IL32以减轻白癜风相关黑素细胞炎症和氧化损伤的治疗前景。
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.
如何引用
AMA
Tianqi Wei, Xin Huang, Jing Zhu, Guanying Liu, Baiyi Zuo, Zhaokang Zhou, et al. Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.. Inflammation. 2026; doi:10.1007/s10753-026-02570-y.
APA
Tianqi Wei, Xin Huang, Jing Zhu, Guanying Liu, Baiyi Zuo, Zhaokang Zhou, et al (2026). Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.. Inflammation. https://doi.org/10.1007/s10753-026-02570-y
GB/T 7714
Tianqi Wei, Xin Huang, Jing Zhu, Guanying Liu, Baiyi Zuo, Zhaokang Zhou, et al. Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.[J]. Inflammation, 2026 doi:10.1007/s10753-026-02570-y.
在 PubMed增强版 阅读全文
翻译全文 · AI 文献问答 · PDF 原文下载 · 引用导出