Mitochondria: sensors and mediators of innate immune receptor signaling

被引：73

作者：

Cloonan, Suzanne M. ^{[1
]}

Choi, Augustine M. K. ^{[1
]}

机构：

[1] Harvard Univ, Brigham & Womens Hosp, Div Pulm & Crit Care Med, Dept Med,Med Sch, Boston, MA 02115 USA

来源：

CURRENT OPINION IN MICROBIOLOGY | 2013年 / 16卷 / 03期

关键词：

NLRP3 INFLAMMASOME ACTIVATION; INDUCED INSULIN-RESISTANCE; TOLL-LIKE RECEPTOR-4; OXIDATIVE STRESS; RIG-I; ANTIVIRAL IMMUNITY; FATTY-ACID; MURINE MACROPHAGES; CROHNS-DISEASE; CELL-DEATH;

D O I：

10.1016/j.mib.2013.05.005

中图分类号：

Q93 [微生物学];

学科分类号：

071005 [微生物学];

摘要：

By integrating stress signals with inputs from other cellular organelles, eukaryotic mitochondria are dynamic sensing systems that can confer substantial impact on innate immune signaling in both health and disease. This review highlights recently discovered elements of innate immune receptor signaling (TLR, RLR, NLR, and CLR) associated with mitochondrial function and discusses the role of mitochondria in the initiation and/or manifestation of inflammatory diseases and disorders. We also highlight the role of mitochondria as therapeutic targets for inflammatory disease.

引用

收藏

页码：327 / 338

页数：12

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