Subversion of Cell-Autonomous Host Defense by Chlamydia Infection

被引:7
|
作者
Fischer, Annette [1 ,2 ]
Rudel, Thomas [1 ,2 ]
机构
[1] Univ Wurzburg, Dept Microbiol, D-97074 Wurzburg, Germany
[2] Univ Wurzburg, Bioctr, D-97074 Wurzburg, Germany
来源
BIOLOGY OF CHLAMYDIA | 2018年 / 412卷
关键词
PATTERN-RECOGNITION RECEPTORS; GAMMA IMMUNE EVASION; TOLL-LIKE RECEPTOR-2; NF-KAPPA-B; APOPTOSIS RESISTANCE; NLRP3; INFLAMMASOME; IFN-GAMMA; TRACHOMATIS INFECTION; CASPASE-1; ACTIVATION; INTERFERON-GAMMA;
D O I
10.1007/82_2016_13
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Obligate intracellular bacteria entirely depend on the metabolites of their host cell for survival and generation of progeny. Due to their lifestyle inside a eukaryotic cell and the lack of any extracellular niche, they have to perfectly adapt to compartmentalized intracellular environment of the host cell and counteract the numerous defense strategies intrinsically present in all eukaryotic cells. This so-called cell-autonomous defense is present in all cell types encountering Chlamydia infection and is in addition closely linked to the cellular innate immune defense of the mammalian host. Cell type and chlamydial species-restricted mechanisms point a long-term evolutionary adaptation that builds the basis of the currently observed host and cell-type tropism among different Chlamydia species. This review will summarize the current knowledge on the strategies pathogenic Chlamydia species have developed to subvert and overcome the multiple mechanisms by which eukaryotic cells defend themselves against intracellular pathogens.
引用
收藏
页码:81 / 106
页数:26
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