World J Gastroenterol. 2010 Apr 21;16(15):1811-9. doi: 10.3748/wjg.v16.i15.1811.
Acute liver failure (ALF) is a devastating clinical syndrome characterised by progressive encephalopathy, coagulopathy, and circulatory dysfunction, which commonly leads to multiorgan failure and death. Central to the pathogenesis of ALF is activation of the immune system with mobilisation of cellular effectors and massive production of cytokines. As key components of the innate immune system, monocytes and macrophages are postulated to play a central role in the initiation, progression and resolution of ALF. ALF in humans follows a rapidly progressive clinical course that poses inherent difficulties in delineating the role of these pivotal immune cells. Therefore, a number of experimental models have been used to study the pathogenesis of ALF. Here we consider the evidence from experimental and human studies of ALF on the role of monocytes and macrophages in acute hepatic injury and the ensuing extrahepatic manifestations, including functional monocyte deactivation and multiple organ failure.
急性肝衰竭（ALF）是一种破坏性的临床综合征，其特征为进行性脑病、凝血障碍和循环功能障碍，通常导致多器官衰竭和死亡。ALF 的发病机制的核心是免疫系统的激活，伴随着细胞效应物的动员和细胞因子的大量产生。单核细胞和巨噬细胞作为固有免疫系统的关键组成部分，被认为在 ALF 的启动、进展和消退中发挥核心作用。人类的 ALF 遵循快速进展的临床过程，这使得阐明这些关键免疫细胞的作用具有内在的困难。因此，已经使用了许多实验模型来研究 ALF 的发病机制。在这里，我们考虑了来自 ALF 的实验和人类研究的证据，这些研究涉及单核细胞和巨噬细胞在急性肝损伤和随后的肝外表现中的作用，包括功能性单核细胞失活和多器官衰竭。
