Department of Dermatovenerology, University of Kragujevac, Faculty of Medical Sciences, Svetozara Markovica 69, 34000 Kragujevac, Serbia.
University Clinical Center Kragujevac, Zmaj Jovina 30, 34000 Kragujevac, Serbia.
Oxid Med Cell Longev. 2022 Mar 12;2022:2249834. doi: 10.1155/2022/2249834. eCollection 2022.
Psoriasis is defined as chronic, immune-mediated disease. Regardless of the development of new therapeutic approaches, the precise etiology of psoriasis remains unknown and speculative. The aim of this review was to systematize the results of previous research on the role of oxidative stress and aberrant immune response in the pathogenesis of psoriasis, as well as the impact of certain therapeutic modalities on the oxidative status in patients with psoriasis. Complex immune pathways of both the innate and adaptive immune systems appear to be major pathomechanisms in the development of psoriasis. Oxidative stress represents another important contributor to the pathophysiology of disease, and the redox imbalance in psoriasis has been reported in skin cells and, systemically, in plasma and blood cells, and more recently, also in saliva. Current immune model of psoriasis begins with activation of immune system in susceptible person by some environmental factor and loss of immune tolerance to psoriasis autoantigens. Increased production of IL-17 appears to be the most prominent role in psoriasis pathogenesis, while IL-23 is recognized as master regulator in psoriasis having a specific role in cross bridging the production of IL-17 by innate and acquired immunity. Other proinflammatory cytokines, including IFN-, TNF-, IL-1, IL-6, IL-22, IL-26, IL-29, or IL-36, have also been reported to play important roles in the development of psoriasis. Oxidative stress can promote inflammation through several signaling pathways. The most noticeable and most powerful antioxidative effects exert various biologics compared to more convenient therapeutic modalities, such as methotrexate or phototherapy. The complex interaction of redox, immune, and inflammatory signaling pathways should be focused on further researches tackling the pathophysiology of psoriasis, while antioxidative supplementation could be the solution in some refractory cases of the disease.
银屑病被定义为一种慢性、免疫介导的疾病。尽管新的治疗方法不断发展,但银屑病的确切病因仍不清楚,目前还只是推测。本综述的目的是系统地总结先前关于氧化应激和异常免疫反应在银屑病发病机制中的作用,以及某些治疗方式对银屑病患者氧化状态的影响的研究结果。先天和适应性免疫系统的复杂免疫途径似乎是银屑病发展的主要发病机制。氧化应激是疾病病理生理学的另一个重要因素,已经在皮肤细胞以及系统地在血浆和血细胞中,最近也在唾液中报道了银屑病中的氧化还原失衡。目前的银屑病免疫模型始于易感个体的免疫系统被某些环境因素激活,以及对银屑病自身抗原失去免疫耐受。IL-17 的产生增加似乎在银屑病发病机制中起着最重要的作用,而 IL-23 被认为是银屑病的主要调节因子,在将先天免疫和获得性免疫产生的 IL-17 联系起来方面具有特定作用。其他促炎细胞因子,包括 IFN-、TNF-、IL-1、IL-6、IL-22、IL-26、IL-29 或 IL-36,也被报道在银屑病的发展中起重要作用。氧化应激可以通过几种信号通路促进炎症。与更方便的治疗方式(如甲氨蝶呤或光疗)相比,各种生物制剂具有更显著和更强大的抗氧化作用。氧化还原、免疫和炎症信号通路的复杂相互作用应成为进一步研究银屑病病理生理学的重点,而抗氧化补充剂可能是某些难治性病例的解决方案。