白癜风中的应激免疫再色素沉着生态位：机制整合和治疗意义
Stress-immune-Repigmentation niche in vitiligo: Mechanistic integration and therapeutic implications.
摘要(中文译文)
白癜风是一种自身免疫性色素脱失性疾病，其特征是选择性黑素细胞丢失和慢性复发过程。越来越多的证据支持了一种网络模型，在该模型中，免疫激活、细胞应激反应和微环境失衡会聚在一起，以驱动疾病活动和再色素沉着稳定性。干扰素-γ驱动的JAK/STAT信号传导诱导趋化因子如CXCL10，并促进CXCR3依赖性细胞毒性T细胞的募集，增强黑素细胞导向的炎症。与此同时，受损的Nrf2介导的抗氧化防御和增强的脂质过氧化降低了黑素细胞的弹性，并可能易患铁下垂，突出了包括SLC3A2、SIRT7和GPX4在内的调节节点作为潜在的应激适应调节因子。持续性和复发越来越多地与IL-15支持的组织驻留记忆T（TRM）细胞和炎症微环境有关，这些微环境可以抑制毛囊黑素细胞干细胞功能，从而破坏再色素沉着。在治疗学上，局部和全身JAK抑制剂已显示出具有临床意义的再色素沉着益处，而针对免疫记忆（如IL-15/TRM途径）和通过Wnt/β-catenin、AhR相关途径和抗氧化/抗铁下垂计划恢复再色素沉着生态位的新兴策略可能会提高耐久性并减少复发。未来的进展将需要生物标志物指导的分层和精心设计的随机试验，以确定在活动性疾病期间阻断主要炎症中心并在维持期间增强黑素细胞弹性的时间组合方案。
Abstract
Vitiligo is an autoimmune depigmenting disorder characterized by selective melanocyte loss and a chronic relapsing course. Increasing evidence supports a network model in which immune activation, cellular stress responses, and microenvironmental imbalance converge to drive disease activity and repigmentation stability. Interferon-γ-driven JAK/STAT signaling induces chemokines such as CXCL10 and promotes CXCR3-dependent recruitment of cytotoxic T cells, reinforcing melanocyte-directed inflammation. In parallel, impaired Nrf2-mediated antioxidant defenses and enhanced lipid peroxidation lower melanocyte resilience and may predispose to ferroptosis, highlighting regulatory nodes including SLC3A2, SIRT7, and GPX4 as potential stress-adaptation regulators. Persistence and recurrence are increasingly linked to IL-15-supported tissue-resident memory T (TRM) cells and inflammatory microenvironments that can suppress hair follicle melanocyte stem cell function, thereby destabilizing repigmentation. Therapeutically, topical and systemic JAK inhibitors have demonstrated clinically meaningful repigmentation benefits, while emerging strategies targeting immune memory (e.g., IL-15/TRM pathways) and restoring the repigmentation niche-through Wnt/β-catenin, AhR-related pathways, and antioxidant/anti-ferroptosis programs-may improve durability and reduce relapse. Future progress will require biomarker-guided stratification and well-designed randomized trials to define temporal combination regimens that block dominant inflammatory hubs during active disease and reinforce melanocyte resilience during maintenance.
如何引用
AMA
Guangman Han, Chang E Chui, Haonan Zhang, Xinyi Yao, Menghan Di, Jing Yuan. Stress-immune-Repigmentation niche in vitiligo: Mechanistic integration and therapeutic implications.. International immunopharmacology. 2026; doi:10.1016/j.intimp.2026.116515.
APA
Guangman Han, Chang E Chui, Haonan Zhang, Xinyi Yao, Menghan Di, Jing Yuan (2026). Stress-immune-Repigmentation niche in vitiligo: Mechanistic integration and therapeutic implications.. International immunopharmacology. https://doi.org/10.1016/j.intimp.2026.116515
GB/T 7714
Guangman Han, Chang E Chui, Haonan Zhang, Xinyi Yao, Menghan Di, Jing Yuan. Stress-immune-Repigmentation niche in vitiligo: Mechanistic integration and therapeutic implications.[J]. International immunopharmacology, 2026 doi:10.1016/j.intimp.2026.116515.
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