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

Trends in immunology · Mar 2011

Review

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

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.

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- Frank L van de Veerdonk, Mihai G Netea, Charles A Dinarello, and Leo A B Joosten.
- Department of Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands. f.veerdonk@aig.umcn.nl
- Trends Immunol. 2011 Mar 1;32(3):110-6.
AbstractInterleukin-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.Copyright © 2011 Elsevier Ltd. All rights reserved.

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