Lu Tian-Fei, Yang Tai-Hua, Zhong Cheng-Peng, Shen Chuan, Lin Wei-Wei, Gu Guang-Xiang, Xia Qiang, Xu Ning
Department of Liver Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medicine School, Hannover 30625, Germany.
Immune Netw. 2018 Jun 28;18(3):e24. doi: 10.4110/in.2018.18.e24. eCollection 2018 Jun.
Ischemia-reperfusion injury (IRI) is a major complication in liver transplantation (LT) and it is closely related to the recovery of grafts' function. Researches has verified that both innate and adaptive immune system are involved in the development of IRI and Kupffer cell (KC), the resident macrophages in the liver, play a pivotal role both in triggering and sustaining the sterile inflammation. Damage-associated molecular patterns (DAMPs), released by the initial dead cell because of the ischemia insult, firstly activate the KC through pattern recognition receptors (PRRs) such as toll-like receptors. Activated KCs is the dominant players in the IRI as it can secret various pro-inflammatory cytokines to exacerbate the injury and recruit other types of immune cells from the circulation. On the other hand, KCs can also serve in a contrary way to ameliorate IRI by upregulating the anti-inflammatory factors. Moreover, new standpoint has been put forward that KCs and macrophages from the circulation may function in different way to influence the inflammation. Managements towards KCs are expected to be the effective way to improve the IRI.
缺血再灌注损伤（IRI）是肝移植（LT）中的主要并发症，且与移植物功能的恢复密切相关。研究已证实，先天性和适应性免疫系统均参与了IRI的发生发展，而肝内常驻巨噬细胞库普弗细胞（KC）在引发和维持无菌性炎症中起关键作用。由于缺血损伤导致的初始死亡细胞释放的损伤相关分子模式（DAMPs），首先通过Toll样受体等模式识别受体（PRRs）激活KC。活化的KC是IRI中的主要参与者，因为它可分泌多种促炎细胞因子以加重损伤，并从循环中募集其他类型的免疫细胞。另一方面，KC也可通过上调抗炎因子以相反的方式减轻IRI。此外，新观点认为循环中的KC和巨噬细胞可能以不同方式影响炎症。针对KC的处理有望成为改善IRI的有效方法。
