Student Research Committee, Alborz University of Medical Sciences, Karaj, Iran.
Department of Immunology and Genetic, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Immunol Invest. 2022 May;51(4):1060-1086. doi: 10.1080/08820139.2021.1878212. Epub 2021 Feb 1.
Interleukin (IL)-33, a member of IL-1 cytokine family, is produced by various immune cells and acts as an alarm to alert the immune system after epithelial or endothelial cell damage during cell necrosis, infection, stress, and trauma. The biological functions of IL-33 largely depend on its ligation to the corresponding receptor, suppression of tumorigenicity 2 (ST2). The pathogenic roles of this cytokine have been implicated in several disorders, including allergic disease, cardiovascular disease, autoimmune disease, infectious disease, and cancers. However, alerted levels of IL-33 may result in either disease amelioration or progression. Genetic variations of gene may confer protective or susceptibility risk in the onset of autoimmune diseases. The purpose of this review is to discuss the involvement of IL-33 and ST2 in the pathogenesis of a variety of autoimmune disorders, such as autoimmune rheumatic, neurodegenerative, and endocrine diseases.
白细胞介素 (IL)-33 是 IL-1 细胞因子家族的成员,由各种免疫细胞产生,在细胞坏死、感染、应激和创伤期间上皮细胞或内皮细胞损伤后充当警报,提醒免疫系统。IL-33 的生物学功能在很大程度上取决于其与相应受体、肿瘤抑制因子 2(ST2)的结合。这种细胞因子的致病作用已涉及多种疾病,包括过敏疾病、心血管疾病、自身免疫性疾病、传染病和癌症。然而,IL-33 的警戒水平可能导致疾病的改善或进展。基因的遗传变异可能在自身免疫性疾病的发病中赋予保护或易感性风险。本综述的目的是讨论 IL-33 和 ST2 在多种自身免疫性疾病发病机制中的作用,如自身免疫性风湿性疾病、神经退行性疾病和内分泌疾病。