白血病抑制因子调节巨噬细胞炎性介质的产生及髓鞘吞噬作用。

Leukemia inhibitory factor modulates production of inflammatory mediators and myelin phagocytosis by macrophages.

作者信息

Hendriks Jerome J A, Slaets Helena, Carmans Sofie, de Vries Helga E, Dijkstra Christine D, Stinissen Piet, Hellings Niels

机构信息

Hasselt University, Biomedical Research Institute (BIOMED), Diepenbeek, Belgium.

出版信息

J Neuroimmunol. 2008 Nov 15;204(1-2):52-7. doi: 10.1016/j.jneuroim.2008.07.015.

DOI:10.1016/j.jneuroim.2008.07.015

PMID:18771807

Abstract

Leukemia inhibitory factor (LIF) promotes survival of glial cells and neurons during autoimmune and injury responses in the central nervous system (CNS). While various studies indicate that LIF also modulates ongoing inflammatory responses, data on underlying events are lacking. In this study we demonstrate that LIF modulates macrophage function. LIF inhibits the production of oxygen radicals and TNFalpha and stimulates myelin uptake by macrophages. These effects of LIF are accompanied by activation of the JAK/STAT3 signalling pathway. Our findings demonstrate that LIF has anti-inflammatory properties and enhances myelin clearance, implicating that LIF may be an important factor in CNS inflammatory disease.

摘要

白血病抑制因子（LIF）在中枢神经系统（CNS）的自身免疫和损伤反应过程中促进神经胶质细胞和神经元的存活。虽然各种研究表明LIF也能调节正在进行的炎症反应，但关于其潜在机制的数据却很缺乏。在本研究中，我们证明LIF可调节巨噬细胞功能。LIF抑制氧自由基和肿瘤坏死因子α（TNFα）的产生，并刺激巨噬细胞摄取髓磷脂。LIF的这些作用伴随着JAK/STAT3信号通路的激活。我们的研究结果表明LIF具有抗炎特性并能增强髓磷脂清除能力，这意味着LIF可能是中枢神经系统炎症性疾病中的一个重要因素。