Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.
Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.
复制标题
DOI：
10.4049/jimmunol.1202443
复制
发表时间：
2013-02-15
期刊：
影响因子：
--
通讯作者：
Fields KA
中科院分区：
文献类型：
--
作者：
Wolf K;Fields KA
I型干扰素在微生物感染期间被诱导，并且具有充分表征的抗病毒活性。TRAF3是一种对I型IFN产生至关重要的信号分子，因此代表了解除免疫应答的潜在靶点。肺炎衣原体是一种人类病原体，主要感染呼吸道上皮细胞，症状发作需要数周，感染过程延长。C.肺炎还与多种慢性炎症性疾病有关。因此，典型的C.人的肺炎感染与对微生物的炎症反应的损害一致。我们证明，上皮细胞感染C。pneumoniae不会导致IFNβ的产生。相反，被感染的细胞被阻止激活IRF3。这种作用是由C. TRAF 3的肺炎依赖性降解，其独立于功能性蛋白酶体。因此，C.肺炎克雷伯氏菌表达靶向TRAF3依赖性免疫效应机制的独特蛋白酶。
Type I interferons are induced during microbial infections and have well characterized anti-viral activities. TRAF3 is a signaling molecule crucial for type I IFN production and therefore represents a potential target for disarming immune responses. Chlamydia pneumoniae is a human pathogen which primarily infects respiratory epithelial cells where onset of symptoms takes several weeks, and the course of infection is protracted. C. pneumoniae has also been associated with a variety of chronic inflammatory conditions. Thus, typical C. pneumoniae infections of humans are consistent with an impairment in inflammatory responses to the microorganism. We demonstrate that infection of epithelial cells with C. pneumoniae does not lead to IFNβ production. Instead, infected cells are prevented from activating IRF3. This effect is mediated by C. pneumoniae-dependent degradation of TRAF3, which is independent of a functional proteasome. Hence it is likely that C. pneumoniae express a unique protease targeting TRAF3-dependent immune effector mechanisms.
登录
查看更多内容
影响因子：
3.1
作者：
Devitt, A;Lund, PA;Pearce, JH
通讯作者：
Pearce, JH
影响因子：
3.6
作者：
Fields, KA;Mead, DJ;Hackstadt, T
通讯作者：
Hackstadt, T
DOI：
10.1016/s0735-1097(98)00016-3
发表时间：
1998-03-15
影响因子：
24
作者：
Maass, M;Bartels, C;Sievers, HH
通讯作者：
Sievers, HH
影响因子：
3.1
作者：
Nagarajan, Uma M.;Prantner, Daniel;Darville, Toni
通讯作者：
Darville, Toni
影响因子：
64.8
作者：
Oganesyan, G;Saha, SK;Cheng, GH
通讯作者：
Cheng, GH