Inflammasomes as Mediators of Immunity Against Influenza Virus

Trends Immunol. 2011 Jan;32(1):34-41. doi: 10.1016/j.it.2010.11.004. Epub 2010 Dec 14.

Abstract

Influenza viruses infect a wide range of avian and mammalian host species including humans. Influenza viruses are a major cause of human respiratory infections and mortality. The innate immune system recognizes influenza viruses through multiple mechanisms. These include endosomal recognition through the Toll-like receptor 7 (TLR7) and cytosolic recognition through the retinoic acid inducible gene I (RIG-I). Recent studies also identified the role of nucleotide binding oligomerization domain (NOD)-like receptors (NLRs) in innate detection of influenza viruses, leading to the activation of the inflammasomes. Here, we review the cellular and molecular mechanisms by which influenza virus infection leads to inflammasome activation, and discuss the consequences of such activation in innate and adaptive immune defense against influenza viruses.

Publication types

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

MeSH terms

  • Adaptive Immunity
  • Animals
  • Humans
  • Immunity, Innate
  • Inflammasomes / immunology*
  • Influenza, Human / immunology*
  • Orthomyxoviridae / physiology*

Substances

  • Inflammasomes