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-1β 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-defici...

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Bibliographic Details
Published inAnnual review of immunology Vol. 29; p. 707
Main Authors Davis, Beckley K, Wen, Haitao, Ting, Jenny P-Y
Format Journal Article
LanguageEnglish
Published United States 23.04.2011
Subjects
Animals
Humans
Inflammasomes - immunology
Inflammation - immunology
Inflammation Mediators - immunology
Intercellular Signaling Peptides and Proteins - immunology
Metabolic Diseases - immunology
Neoplasms - immunology
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Summary:Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1β 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.
ISSN:1545-3278
DOI:10.1146/annurev-immunol-031210-101405