Kornfeld H, Mancino G, Colizzi V
The Pulmonary Center, Boston University School of Medicine, 80 East Concord Street, Boston, Masachusetts, USA.
Cell Death Differ. 1999 Jan;6(1):71-8. doi: 10.1038/sj.cdd.4400454.
Studies of host responses to infection have traditionally focused on the direct antimicrobial activity of effector molecules (antibodies, complement, defensins, reactive oxygen and nitrogen intermediates) and immunocytes (macrophages, lymphocytes, and neutrophils among others). The discovery of the systems for programmed cell death of eukaryotic cells has revealed a unique role for this process in the complex interplay between microorganisms and their cellular targets or responding immunocytes. In particular, cells of the monocyte/macrophage lineage have been demonstrated to undergo apoptosis following intracellular infection with certain pathogens that are otherwise capable of surviving within the hostile environment of the phagosome or which can escape the phagosome. Mycobacterium tuberculosis is a prototypical 'intracellular parasite' of macrophages, and the direct induction of macrophage apoptosis by this organism has recently been reported from several laboratories. This paper reviews the current understanding of the mechanism and regulation of macrophage apoptosis in response to M. tuberculosis and examines the role this process plays in protective immunity and microbial virulence.
对宿主感染反应的研究传统上集中于效应分子（抗体、补体、防御素、活性氧和氮中间体）和免疫细胞（巨噬细胞、淋巴细胞及中性粒细胞等）的直接抗菌活性。真核细胞程序性细胞死亡系统的发现揭示了这一过程在微生物与其细胞靶点或反应性免疫细胞之间复杂相互作用中的独特作用。特别是，单核细胞/巨噬细胞系的细胞在受到某些病原体的细胞内感染后会发生凋亡，这些病原体在吞噬体的恶劣环境中能够存活，或者能够逃离吞噬体。结核分枝杆菌是巨噬细胞的典型“细胞内寄生虫”，最近几个实验室报道了该菌对巨噬细胞凋亡的直接诱导作用。本文综述了目前对结核分枝杆菌感染后巨噬细胞凋亡机制及调控的认识，并探讨了这一过程在保护性免疫和微生物毒力中所起的作用。
