The inflammasome NLRs in immunity, inflammation, and associated diseases

Annu Rev Immunol. 2011;29:707-35. doi: 10.1146/annurev-immunol-031210-101405.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammasomes / immunology*
  • Inflammation / immunology*
  • Inflammation Mediators / immunology
  • Intercellular Signaling Peptides and Proteins / immunology*
  • Metabolic Diseases / immunology
  • Neoplasms / immunology

Substances

  • Inflammasomes
  • Inflammation Mediators
  • Intercellular Signaling Peptides and Proteins