Evasion of inflammasome activation by microbial pathogens

被引:54
|
作者
Ulland, Tyler K. [1 ,2 ]
Ferguson, Polly J. [3 ]
Sutterwala, Fayyaz S. [1 ,2 ,4 ,5 ]
机构
[1] Univ Iowa, Inflammat Program, Iowa City, IA USA
[2] Univ Iowa, Interdisciplinary Program Mol & Cellular Biol, Iowa City, IA USA
[3] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA
[4] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA
[5] Vet Affairs Med Ctr, Iowa City, IA 52242 USA
来源
JOURNAL OF CLINICAL INVESTIGATION | 2015年 / 125卷 / 02期
关键词
INTERLEUKIN-1 RECEPTOR ANTAGONIST; PLACEBO-CONTROLLED TRIAL; JUVENILE IDIOPATHIC ARTHRITIS; TYPE-2; DIABETES-MELLITUS; III SECRETION SYSTEM; ONSET STILLS-DISEASE; LONG-TERM SAFETY; RHEUMATOID-ARTHRITIS; DOUBLE-BLIND; FRANCISELLA-TULARENSIS;
D O I
10.1172/JCI75254
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Activation of the inflammasome occurs in response to infection with a wide array of pathogenic microbes. The inflammasome serves as a platform to activate caspase-1, which results in the subsequent processing and secretion of the proinflammatory cytokines IL-1 beta and IL-18 and the initiation of an inflammatory cell death pathway termed pyroptosis. Effective inflammasome activation is essential in controlling pathogen replication as well as initiating adaptive immune responses against the offending pathogens. However, a number of pathogens have developed strategies to evade inflammasome activation. In this Review, we discuss these pathogen evasion strategies as well as the potential infectious complications of therapeutic blockade of IL-1 pathways.
引用
收藏
页码:469 / 477
页数:9
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