Yang Feifei, Zhu Ping, Duan Lihua, Yang Lin, Wang Jiajun
Department of Nephrology, The First College of Clinical Medical Science, Three Gorges University, Yichang, Hubei 443003, P.R. China.
Department of Rheumatology and Clinical Immunology, The First Hospital of Xiamen University, Xiamen, Fujian 361000, P.R. China.
Mol Med Rep. 2016 Jan;13(1):3-8. doi: 10.3892/mmr.2015.4516. Epub 2015 Nov 6.
Interleukin (IL)-33, is a novel member of the IL-1 superfamily, and act as a dual-function molecule as a nuclear factor and cytokine. The expression of IL-33 can be detected in several tissues and cells in humans and in mice. In addition to the conventional secretion approach for cytokines, full-length IL-33 can also be released into the extracellular space following cell damage or mechanical injury. IL-33 mediates its biological effects by interacting with the receptors, suppression of tumorigenicity 2 (ST2) and IL-1 receptor accessory protein, activating intracellular molecules in the nuclear factor-κB and mitogen-activated protein kinase signaling pathways, which drive the production of type 2 cytokines, including IL-4, IL-5 and IL-3, from polarized T helper 2 cells. Increasing evidence indicates that IL-33 is important in chronic kidney disease, and may be involved in the progression of renal fibrosis associated with systemic lupus erythematosus and renal graft damage. In addition, IL-33 contributes to acute kidney injury. In the present review, the biology of IL-33, and the association of IL-33 with kidney diseases are discussed.
白细胞介素（IL）-33是IL-1超家族的一个新成员，作为一种核因子和细胞因子发挥双重功能分子的作用。在人和小鼠的多种组织和细胞中均可检测到IL-33的表达。除了细胞因子的传统分泌方式外，全长IL-33在细胞损伤或机械损伤后也可释放到细胞外空间。IL-33通过与受体、抑瘤2（ST2）和IL-1受体辅助蛋白相互作用来介导其生物学效应，激活核因子-κB和丝裂原活化蛋白激酶信号通路中的细胞内分子，从而驱动极化的辅助性T细胞2产生2型细胞因子，包括IL-4、IL-5和IL-3。越来越多的证据表明，IL-33在慢性肾脏病中起重要作用，可能参与系统性红斑狼疮相关的肾纤维化进展和肾移植损伤。此外，IL-33还与急性肾损伤有关。在本综述中，将讨论IL-33的生物学特性以及IL-33与肾脏疾病的关联。
