Inflammasome activation and IL-1beta and IL-18 processing during infection
until further notice
SourceTrends in Immunology, 32, 3, (2011), pp. 110-6
Article / Letter to editor
Display more detailsDisplay less details
Trends in Immunology
SubjectN4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity
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.
Upload full text
Use your RU credentials (u/z-number and password) to log in with SURFconext to upload a file for processing by the repository team.