Vitiligo is an autoimmune disease of the skin characterized by epidermal melanocyte loss resulting in white patches, with an approximate prevalence of 0.5–2% worldwide. Several precipitating factors by chemical exposure and skin injury present commonly in patients with vitiligo. Although the diagnosis appears to be straightforward for the distinct clinical phenotype and specific histological features, vitiligo provides many challenges including chronicity, treatment resistance, frequent relapse, associated profound psychosocial effect, and negative impact on quality of life. Multiple mechanisms are involved in melanocyte disappearance, including genetics, environmental factors, and immune-mediated inflammation. Compelling evidence supports the melanocyte intrinsic abnormalities with poor adaptation to stressors leading to instability and release of danger signals, which will activate dendritic cells, natural killer cells, and innate lymphoid cells to initiate innate immunity, ultimately resulting in T-cell mediated adaptive immune response and melanocyte destruction. Importantly, the cross- talk between keratinocytes, melanocytes, and immune cells, such as interferon (IFN)-γ signaling pathway, builds inflammatory loops that give rise to the disease deterioration. Improved understanding of the immune pathogenesis of vitiligo has led to the development of new therapeutic options including Janus kinase (JAK) inhibitors targeting IFN-γ signaling pathways, which can effectively reverse depigmentation. Furthermore, definition of treatment goals and integration of comorbid diseases into vitiligo management have revolutionized the way vitiligo is treated. In this review, we highlight recent developments in vitiligo clinical aspects and immune pathogenesis. Our key objective is to raise awareness of the complexity of this disease, the potential of prospective therapy strategies, and the need for early and comprehensive management.

白癜风是一种皮肤自身免疫性疾病，其特征是表皮黑色素细胞丢失导致白色斑块，全球患病率约为 0.5-2%。白癜风患者中常见的几种化学暴露和皮肤损伤的诱发因素。尽管针对不同的临床表型和特定的组织学特征，诊断似乎很简单，但白癜风带来了许多挑战，包括慢性病、治疗抗性、频繁复发、相关的深刻社会心理影响以及对生活质量的负面影响。黑素细胞消失涉及多种机制，包括遗传、环境因素和免疫介导的炎症。令人信服的证据支持黑色素细胞内在异常对应激源的适应性差导致不稳定和释放危险信号，这将激活树突状细胞、自然杀伤细胞和先天淋巴细胞以启动先天免疫，最终导致 T 细胞介导的适应性免疫反应和黑素细胞破坏。重要的是，角质形成细胞、黑色素细胞和免疫细胞之间的相互作用，如干扰素 (IFN)-γ 信号通路，会形成导致疾病恶化的炎症循环。对白癜风免疫发病机制的深入了解导致了新的治疗选择的发展，包括针对 IFN-γ 信号通路的 Janus 激酶 (JAK) 抑制剂，它可以有效地逆转色素脱失。此外，治疗目标的定义以及将合并症纳入白癜风管理已经彻底改变了白癜风的治疗方式。在这篇综述中，我们重点介绍了白癜风临床方面和免疫发病机制的最新进展。我们的主要目标是提高人们对这种疾病的复杂性、前瞻性治疗策略的潜力以及早期和全面管理的必要性的认识。