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Title: Inflammasome activation and IL-1beta and IL-18 processing during infection
Author(s): Veerdonk, F.L. van de ; Netea, M.G. ; Dinarello, C.A. ; Joosten, L.A.B.
Publication year: 2011
Source: Trends in Immunology, vol. 32, iss. 3, (2011), pp. 110-116
ISSN: 1471-4906
DOI: http://dx.doi.org/10.1016/j.it.2011.01.003
Publication type: Article / Letter to editor

Please use this identifier to cite or link to this item : https://hdl.handle.net/2066/98006   https://hdl.handle.net/2066/98006

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Subject: N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity
Organization: Internal Medicine
Journal title:
Trends in Immunology
Volume: vol. 32
Issue: iss. 3
Page start: p. 110
Page end: p. 116
Abstract:
Interleukin-1beta (IL-1beta) 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-1beta 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-1beta 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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