Paganelli Alessia, Cristofoletti Cristina, Moro Francesco, Corrente Alessandra, Colonna Laura, Scala Emanuele, Picardo Mauro
Dermatology Unit, Istituto Dermopatico dell'Immacolata-Istituto di Ricovero e Cura a Carattere Scientifico (IDI-IRCCS), via dei Monti di Creta 104, 00167 Rome, Italy.
Clinical Trial Center, Istituto Dermopatico dell'Immacolata-Istituto di Ricovero e Cura a Carattere Scientifico (IDI-IRCCS), 00167 Rome, Italy.
Life (Basel). 2025 Apr 23;15(5):684. doi: 10.3390/life15050684.
(1) Background: Vitiligo is an autoimmune skin disorder characterized by melanocyte destruction. Despite metabolic disturbances and oxidative stress also playing a key role in its pathogenesis, accumulating evidence highlights a prominent role for cytokine dysregulation. (2) Methods: A systematic search was conducted to identify meta-analyses published in the last decade that investigated cytokine involvement in vitiligo. (3) Results: Based on predefined inclusion criteria, nine meta-analyses were retrieved and reviewed. The findings confirm a central role for interferon-gamma (IFN-γ) in vitiligo pathogenesis, although recent meta-analyses suggest that IFN-γ gene polymorphisms are more broadly associated with autoimmunity rather than being vitiligo-specific. Elevated interleukin-17 (IL-17) levels have been consistently reported in vitiligo patients, supporting its contribution to immune-mediated melanocyte destruction. Regulatory T cell dysfunction appears to play a crucial role in disease progression. Additionally, TNF-α-308 G/A polymorphism has been linked to a genetic susceptibility to vitiligo, particularly in specific populations, reinforcing the role of TNF-α in immune dysregulation. Lastly, chemokines involved in immune cell recruitment to melanocytes further illustrate the complex inflammatory network underlying the disease. (4) Conclusions: This systematic review consolidates evidence from a decade of meta-analyses, underscoring the significance of cytokine dysregulation in vitiligo and highlighting potential therapeutic targets.
（1）背景：白癜风是一种以黑素细胞破坏为特征的自身免疫性皮肤病。尽管代谢紊乱和氧化应激在其发病机制中也起关键作用，但越来越多的证据表明细胞因子失调起着突出作用。（2）方法：进行系统检索，以确定过去十年发表的调查细胞因子与白癜风关系的荟萃分析。（3）结果：根据预先确定的纳入标准，检索并综述了9项荟萃分析。研究结果证实干扰素-γ（IFN-γ）在白癜风发病机制中起核心作用，尽管最近的荟萃分析表明IFN-γ基因多态性与自身免疫的关联更为广泛，而非白癜风特异性。白癜风患者中白细胞介素-17（IL-17）水平持续升高，支持其对免疫介导的黑素细胞破坏的作用。调节性T细胞功能障碍似乎在疾病进展中起关键作用。此外，TNF-α -308 G/A多态性与白癜风的遗传易感性有关，尤其是在特定人群中，强化了TNF-α在免疫失调中的作用。最后，参与免疫细胞向黑素细胞募集的趋化因子进一步说明了该疾病潜在的复杂炎症网络。（4）结论：本系统综述整合了过去十年荟萃分析的证据，强调了细胞因子失调在白癜风中的重要性，并突出了潜在的治疗靶点。
