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

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• 作者：Frank L. van de Veerdonk¹ ; ² ; ^{f.veerdonk@aig.umcn.nl} ; Mihai G. Netea¹ ; ² ; Charles A. Dinarello² ; ³ ; Leo A.B. Joosten¹ ; ²
• 刊名：Trends in Immunology
• 出版年：2011
• 出版时间：March 2011
• 年：2011
• 卷：32
• 期：3
• 页码：110-116
• 全文大小：423 K

文摘

Interleukin-1β (IL-1β) 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-1β 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-1β 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.