Chen Jie, He Yan, Xie Zhongming, Wei Yingying, Duan Lihua
Department of Scientific Research and Education, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, Jiangxi, China.
Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China.
Cardiol Res Pract. 2020 Mar 19;2020:6108362. doi: 10.1155/2020/6108362. eCollection 2020.
Interleukin-33 (IL-33) is a member of the IL-1 family of proteins that are produced by a variety of cell types in multiple tissues. Under conditions of cell injury or death, IL-33 is passively released from the nucleus and acts as an "alarmin" upon binding to its specific receptor ST2, which leads to proinflammatory or anti-inflammatory effects depending on the pathological environment. To date, numerous studies have investigated the roles of IL-33 in human and murine models of diseases of the nervous system, digestive system, pulmonary system, as well as other organs and systems, including solid organ transplantation. With graft rejection and ischemia-reperfusion injury being the most common causes of grafted organ failure or dysfunction, researchers have begun to investigate the role of IL-33 in the immune-related mechanisms of graft tolerance and rejection using heart transplantation models. In the present review, we summarize the identified roles of IL-33 as well as the corresponding mechanisms by which IL-33 acts within the progression of graft rejection after heart transplantation in animal models.
白细胞介素-33（IL-33）是IL-1蛋白家族的成员，由多种组织中的多种细胞类型产生。在细胞损伤或死亡的情况下，IL-33从细胞核中被动释放，与其特异性受体ST2结合后作为一种“警报素”发挥作用，根据病理环境导致促炎或抗炎作用。迄今为止，许多研究已经在人类和小鼠的神经系统、消化系统、肺部系统以及包括实体器官移植在内的其他器官和系统疾病模型中研究了IL-33的作用。由于移植排斥和缺血再灌注损伤是移植器官衰竭或功能障碍的最常见原因，研究人员已经开始使用心脏移植模型研究IL-33在移植耐受和排斥的免疫相关机制中的作用。在本综述中，我们总结了IL-33在动物模型心脏移植后移植排斥进展过程中已确定的作用以及IL-33发挥作用的相应机制。
