Chlamydia trachomatis can protect host cells against apoptosis in the absence of cellular Inhibitor of Apoptosis Proteins and Mcl-1

被引:17
作者
Ying, Songmin [1 ]
Christian, Jan G. [1 ]
Paschen, Stefan A. [1 ]
Haecker, Georg [1 ]
机构
[1] Tech Univ Munich, Inst Med Microbiol Immunol & Hyg, D-81675 Munich, Germany
关键词
Chlamydia; apoptosis; Caspases; inhibitor of apoptosis proteins;
D O I
10.1016/j.micinf.2007.10.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Infection with Chlamydia protects mammalian host cells against apoptosis. Hypotheses have been proposed to explain this molecularly, including the up-regulation of host anti-apoptotic proteins such as cellular Inhibitor of Apoptosis Protein (IAP) 2 and the Bcl-2 protein Mcl-l. To test for the importance of these proteins, we used mouse embryonic fibroblasts from gene-targeted mice that were deficient in cIAPl, cIAP2, cIAPI /cIAP2, XIAP, or Mcl-1. Infection with Chlamydia trachomatis protected all cells equally well against apoptosis, which was induced either with tumour necrosis factor/cycloheximide (IAP-knock-out cells) or staurosporine (Mcl-1-knock-out). Therefore, these cellular anti-apoptotic proteins are not essential for apoptosis-protection by C. trachomatis. (c) 2007 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:97 / 101
页数:5
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