Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China (mainland).
Department of Dermatology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, China (mainland).
Med Sci Monit. 2019 Feb 6;25:1017-1023. doi: 10.12659/MSM.914898.
Vitiligo is an autoimmune cutaneous disease in which melanocytes are destroyed by CD8⁺ T cells resulting in disfiguring white spots. From the very beginning of the disease, oxidative stress plays a significant role in promoting the onset of vitiligo, as noted by many studies. Multiple factors lead to the overproduction of reactive oxygen species (ROS), and collaboratively cause ROS accumulation in vulnerable melanocytes. However, ROS are responsible for melanocyte damage manifested by the level of molecules, organelles, and cells, and the generation of autoantigens, through different pathways related to the dysregulation of melanocytes. Recent studies have shown that presentation of autoantigens is mediated by innate immunity, which bridges the gap between oxidative stress and adaptive immunity. The recruitment of CD8⁺ T cells induced by cytokines and chemokines guarantees the final destruction of epidermal melanocytes. Moreover, emerging concerns regarding regulatory T cells and resident memory T cells help explain the reinstatement and relapse of vitiligo. Here, we provide new perspectives in the advances in understanding of this disease pathogenesis and we attempt to find more interrelationships between oxidative stress and autoimmunity.
白癜风是一种自身免疫性皮肤疾病，其中黑素细胞被 CD8+T 细胞破坏，导致出现令人毁容的白色斑点。正如许多研究指出的那样，从疾病一开始，氧化应激就在促进白癜风的发生中起着重要作用。多种因素导致活性氧（ROS）的过度产生，并协同导致易受伤害的黑素细胞中 ROS 的积累。然而，ROS 通过与黑素细胞失调相关的不同途径导致黑素细胞损伤，表现为分子、细胞器和细胞水平的损伤，以及自身抗原的产生。最近的研究表明，自身抗原的呈递是由先天免疫介导的，它填补了氧化应激和适应性免疫之间的空白。细胞因子和趋化因子招募的 CD8+T 细胞保证了表皮黑素细胞的最终破坏。此外，关于调节性 T 细胞和驻留记忆 T 细胞的新关注点有助于解释白癜风的复发和再发。在这里，我们提供了对该疾病发病机制的理解方面的新进展的视角，并试图发现氧化应激和自身免疫之间的更多相互关系。
