Mycobacterium tuberculosis phagosome maturation arrest:: Selective targeting of PI3P-dependent membrane trafficking

被引：83

作者：

Vergne, I

Chua, J

Deretic, V ^{[1
]}

机构：

[1] Univ New Mexico, Sch Med, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA

[2] Univ New Mexico, Sch Med, Dept Cell Biol & Physiol, Albuquerque, NM 87131 USA

来源：

TRAFFIC | 2003年 / 4卷 / 09期

关键词：

calcium; phagosome; phosphatidylinositol; 3-kinase; trans-Golgi-network; tuberculosis;

D O I：

10.1034/j.1600-0854.2003.00120.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The ability of Mycobacterium tuberculosis to enter host macrophages, and reside in a phagosome, which does not mature into a phagolysosome, is central to the spread of tuberculosis and the associated pandemic involving billions of people worldwide. Tuberculosis can be viewed as a disease with a significant intracellular trafficking and organellar biogenesis component. Current understanding of the block in M. tuberculosis phagosome maturation also sheds light on fundamental aspects of phagolysosome biogenesis. The maturation block involves interference with the recruitment and function of rabs, rab effectors (phosphatidylinositol 3-kinases and tethering molecules such as EEA1), SNAREs (Syntaxin 6 and cellubrevin) and Ca2+ /calmodulin signaling. M. tuberculosis analogs of mammalian phosphatidylinositols interfere with these systems and associated processes.

引用

页码：600 / 606

页数：7

共 56 条

[31] Mycobacterium tuberculosis phagosomes exhibit altered calmodulin-dependent signal transduction:: Contribution to inhibition of phagosome-lysosome fusion and intracellular survival in human macrophages [J].