Inflammasome activation and IL-1β and IL-18 processing during infection

被引：565

作者：

de Veerdonk, Frank L. van ^{[1
,2
]}

Netea, Mihai G. ^{[1
,2
]}

Dinarello, Charles A. ^{[2
,3
]}

Joosten, Leo A. B. ^{[1
,2
]}

机构：

[1] Radboud Univ Nijmegen, Med Ctr, Dept Med, NL-6525 ED Nijmegen, Netherlands

[2] Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Infect Inflammat & Immun, NL-6525 ED Nijmegen, Netherlands

[3] Univ Colorado Denver, Div Infect Dis, Aurora, CO USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 03期

关键词：

NLRP3; INFLAMMASOME; NALP3; P2X(7) RECEPTOR; HOST-DEFENSE; CASPASE-1; CELLS; INTERLEUKIN-1-BETA; RECOGNITION; SECRETION; DEFICIENT;

D O I：

10.1016/j.it.2011.01.003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Interleukin-1 beta (IL-1 beta) and IL-18 contribute to host defense against infection by augmenting antimicrobial properties of phagocytes and initiating Th1 and Th17 adaptive immune responses. Protein complexes called inflammasomes activate intracellular caspase-1 autocatalytically, which cleaves the inactive precursors of IL-1 beta and IL-18 into bioactive cytokines. In this review, we discuss the controversies regarding inflammasome activation and the role of the inflammasome during infection. We highlight alternative mechanisms for processing IL-1 beta and IL-18 during infection, which involve extracellular cleavage of the inactive cytokines by neutrophil-derived serine proteases or proteases released from cytotoxic T cells.

引用

页码：110 / 116

页数：7

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