中文摘要：

淋巴细胞的激活诱导细胞死亡（AICD）的分子机制已经得到了广泛的研究。巨噬细胞中也存在AICD，但是诱导巨噬细胞AICD的分子机理仍不是很清楚。最近，一些研究表明zVAD或IFNT通过提高MEF2C蛋白稳定性，从而增加其在巨噬细胞中的含量。MEF2C和TLR2、4信号通路一起，诱导了Nur77的表达。Nur77的表达介导了巨噬细胞的凋亡。LPS激活的ERK和p38是诱导Nur77表达和细胞凋亡所必需的。p38／STAT1／ROS途径也介导了巨噬细胞的AICD。撤除血清诱导的巨噬细胞凋亡可能是一种新的巨噬细胞AICD模型。这些发现将有助于我们对巨噬细胞AICD的进一步了解。

英文摘要：

Molecular mechanism of AICD （activation induced cell death） in lymphocytes has been extensively studied. AICD also occurs in macrophages. However, the signaling pathways that are involved in macrophage AICD remains uncertain. Recently, ours and others＇ studies reveal that zVAD or IFNγ induces the increase of MEF2C protein, possibly by increasing its protein stability. MEF2C, together with TLR2 and TLR4 signaling, induces Nur77 expression leading macrophage to death. LPS- activated ERK and p38 also mediate Nut77 expression, p38/STAT1/ROS pathway contribute to AICD of macrophage as well. Serum-deprivation induced macrophage apoptosis is identified as one kind of macrophage＇s AICD. These finding will help to better understand the mechanism of AICD in macrophages.