Inflammasomes as mediators of immunity against influenza virus

被引：127

作者：

Pang, Iris K. ^{[1
]}

Iwasaki, Akiko ^{[1
]}

机构：

[1] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06520 USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 01期

基金：

美国国家卫生研究院;

关键词：

ION-CHANNEL ACTIVITY; T-CELL RESPONSES; DOUBLE-STRANDED-RNA; NF-KAPPA-B; A-VIRUS; NLRP3; INFLAMMASOME; CUTTING EDGE; HOST-DEFENSE; ANTIVIRAL RESPONSES; RECEPTOR ANTAGONIST;

D O I：

10.1016/j.it.2010.11.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Influenza viruses infect a wide range of avian and mammalian host species including humans. Influenza viruses are a major cause of human respiratory infections and mortality. The innate immune system recognizes influenza viruses through multiple mechanisms. These include endosomal recognition through the Toll-like receptor 7 (TLR7) and cytosolic recognition through the retinoic acid inducible gene I (RIG-I). Recent studies also identified the role of nucleotide binding oligomerization domain (NOM-like receptors (NLRs) in innate detection of influenza viruses, leading to the activation of the inflammasomes. Here, we review the cellular and molecular mechanisms by which influenza virus infection leads to inflammasome activation, and discuss the consequences of such activation in innate and adaptive immune defense against influenza viruses.

引用

页码：34 / 41

页数：8

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