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The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1ββ and pro-IL-18 among other substrates. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

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Publisher
Annual Reviews
Copyright
Copyright ©© 2011 by Annual Reviews. All rights reserved
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev-immunol-031210-101405
pmid
21219188
Publisher site
See Article on Publisher Site

Abstract

Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1ββ and pro-IL-18 among other substrates. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 23, 2011

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