Departamento de Medicina Interna, Hospital Universitario "Dr. José E. González", Universidad Autónoma de Nuevo León, Madero y Gonzalitos S/N, Monterrey, NL, 64700, Mexico,
Am J Clin Dermatol. 2013 Oct;14(5):343-50. doi: 10.1007/s40257-013-0039-3.
Vitiligo is an acquired immune disorder of the skin characterized by the presence of white depigmented macules. Its immunopathogenesis is not completely understood, but inflammatory alterations in the skin microenvironment, and particularly increased expression of the cytokine tumor necrosis factor-α (TNFα), are thought to be essential regulators of melanocyte dysfunction and death. In this article we review the evidence that implicates TNFα in the pathogenesis of vitiligo, including studies on serum and tissue levels of TNFα, TNFα gene polymorphisms, in vitro studies, and therapeutic trials using TNFα inhibitors. TNFα emerges as a complex mediator with apparently conflicting roles in vitiligo.
白癜风是一种获得性皮肤免疫紊乱，其特征是存在白色色素减退斑。其免疫发病机制尚不完全清楚，但皮肤微环境的炎症改变，特别是细胞因子肿瘤坏死因子-α（TNFα）的表达增加，被认为是调节黑色素细胞功能障碍和死亡的重要因素。本文综述了 TNFα在白癜风发病机制中的作用的证据，包括血清和组织 TNFα水平、TNFα 基因多态性、体外研究以及 TNFα 抑制剂的治疗试验。TNFα 作为一种复杂的介质，在白癜风中表现出明显矛盾的作用。
