Document Detail

IL-1beta processing in host defense: beyond the inflammasomes.
MedLine Citation:
PMID:  20195505     Owner:  NLM     Status:  MEDLINE    
Stimulation and release of proinflammatory cytokines is an essential step for the activation of an effective innate host defense, and subsequently for the modulation of adaptive immune responses. Interleukin-1beta (IL-1beta) and IL-18 are important proinflammatory cytokines that on the one hand activate monocytes, macropages, and neutrophils, and on the other hand induce Th1 and Th17 adaptive cellular responses. They are secreted as inactive precursors, and the processing of pro-IL-1beta and pro-IL-18 depends on cleavage by proteases. One of the most important of these enzymes is caspase-1, which in turn is activated by several protein platforms called the inflammasomes. Inflammasome activation differs in various cell types, and knock-out mice defective in either caspase-1 or inflammasome components have an increased susceptibility to several types of infections. However, in other infections and in models of sterile inflammation, caspase-1 seems to be less important, and alternative mechanisms such as neutrophil-derived serine proteases or proteases released from microbial pathogens can process and activate IL-1beta. In conclusion, IL-1beta/IL-18 processing during infection is a complex process in which the inflammasomes are only one of several activation mechanisms.
Mihai G Netea; Anna Simon; Frank van de Veerdonk; Bart-Jan Kullberg; Jos W M Van der Meer; Leo A B Joosten
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-02-26
Journal Detail:
Title:  PLoS pathogens     Volume:  6     ISSN:  1553-7374     ISO Abbreviation:  PLoS Pathog.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-03-02     Completed Date:  2010-04-27     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  101238921     Medline TA:  PLoS Pathog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1000661     Citation Subset:  IM    
Department of Medicine, Radboud University Nijmegen Medical Center, and Nijmegen Center for Infections, Inflammation and Immunity (N4i), Nijmegen, The Netherlands.
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MeSH Terms
Inflammation / immunology*
Inflammation Mediators / immunology*
Interleukin-18 / immunology*
Interleukin-1beta / immunology*
Signal Transduction / immunology*
Reg. No./Substance:
0/Inflammation Mediators; 0/Interleukin-18; 0/Interleukin-1beta

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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