Mechanisms and Functions of Inflammasomes

被引：2238
作者：
Lamkanfi, Mohamed [1 ,2 ]
Dixit, Vishva M. [3 ]
机构：
[1] VIB, Dept Med Prot Res, B-9000 Ghent, Belgium
[2] Univ Ghent, Dept Biochem, B-9000 Ghent, Belgium
[3] Genentech Inc, Dept Physiol Chem, San Francisco, CA 94080 USA
来源：
CELL | 2014年 / 157卷 / 05期
基金：
欧洲研究理事会;
关键词：
COLD AUTOINFLAMMATORY SYNDROME; III SECRETION APPARATUS; ANTHRAX LETHAL TOXIN; LONG-TERM EFFICACY; NLRP3; INFLAMMASOME; MACULAR DEGENERATION; NALP3; HOST-DEFENSE; CELL-DEATH; INTERLEUKIN-1-BETA SECRETION;
D O I：
10.1016/j.cell.2014.04.007
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1 beta and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field.
引用
收藏
页码：1013 / 1022
页数：10
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