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急性肝衰竭中巨噬细胞的演变故事。

The evolving story of macrophages in acute liver failure.

机构信息

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, Medical College, Zhejiang University, Zhejiang, PR China.

出版信息

Immunol Lett. 2012 Sep;147(1-2):1-9. doi: 10.1016/j.imlet.2012.07.002. Epub 2012 Jul 20.

Abstract

Acute liver failure (ALF) remains a worldwide problem. The innate immune system acts as an important regulator of ALF. Kupffer cells (KCs), the resident macrophages in liver, play a key role in liver innate immune response. Recent researches have shown that macrophages display a remarkable plasticity and can differentiate into functionally diverse subsets. However, the dynamic polarized phenotypes and functional status of macrophages at different stage of ALF are not clear. In this paper, we present a review of evidence that KCs play a significant role in the pathogenesis of ALF, including the phenotype and functions of macrophages, signaling pathways involved in macrophage functional status and cell-crosstalks of KCs with other immune cells. More information on macrophages will promote a better understanding of the cellular molecular mechanisms of ALF and provide new insights for the development of therapeutic targets for ALF.

摘要

急性肝衰竭(ALF)仍然是一个全球性的问题。先天免疫系统是 ALF 的重要调节者。库普弗细胞(KCs),即肝脏中的常驻巨噬细胞,在肝脏先天免疫反应中发挥关键作用。最近的研究表明,巨噬细胞表现出显著的可塑性,并能分化为功能不同的亚群。然而,在 ALF 的不同阶段,巨噬细胞的动态极化表型和功能状态尚不清楚。本文综述了 KCs 在 ALF 发病机制中的重要作用的证据,包括巨噬细胞的表型和功能、参与巨噬细胞功能状态的信号通路以及 KCs 与其他免疫细胞的细胞串扰。更多关于巨噬细胞的信息将促进对 ALF 细胞分子机制的更好理解,并为 ALF 的治疗靶点的发展提供新的见解。

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