Hestvik Anne Lise K, Hmama Zakaria, Av-Gay Yossef
Department of Medicine, Division of Infectious Diseases, University of British Columbia, Vancouver, British Columbia, 2733 Heather St. Vancouver, BC, Canada V5Z 3J5.
FEMS Microbiol Rev. 2005 Nov;29(5):1041-50. doi: 10.1016/j.femsre.2005.04.013. Epub 2005 Jul 1.
Phagosome biogenesis, the process by which macrophages neutralize ingested pathogens and initiate antigen presentation, has entered the field of cellular mycobacteriology research largely owing to the discovery 30 years ago that phagosomes harboring mycobacteria are refractory to fusion with lysosomes. In the past decade, the use of molecular genetics and biology in different model systems to study phagosome biogenesis have made significant advances in understanding subtle mechanisms by which mycobacteria inhibit the maturation of its phagosome. Thus, we are beginning to appreciate the extent to which these pathogens are able to interfere with innate immune responses and manipulate defense mechanisms to enhance their survival within the human host cell. Here, we summarize current knowledge about phagosome maturation arrest in infected macrophages and the subsequent attenuation of the macrophage-initiated adaptive anti-mycobacterial immune defenses.
吞噬体生物发生是巨噬细胞中和摄入病原体并启动抗原呈递的过程,主要由于30年前的一项发现,即含有分枝杆菌的吞噬体难以与溶酶体融合,这一过程已进入细胞分枝杆菌学研究领域。在过去十年中,利用分子遗传学和生物学在不同模型系统中研究吞噬体生物发生,在理解分枝杆菌抑制其吞噬体成熟的微妙机制方面取得了重大进展。因此,我们开始认识到这些病原体能够在多大程度上干扰先天免疫反应并操纵防御机制,以增强它们在人类宿主细胞内的生存能力。在这里,我们总结了目前关于感染巨噬细胞中吞噬体成熟停滞以及随后巨噬细胞启动的适应性抗分枝杆菌免疫防御减弱的知识。