Autophagy limits activation of the inflammasomes

Immunol Rev. 2018 Jan;281(1):62-73. doi: 10.1111/imr.12613.


Inflammasomes are multiprotein complexes that control the maturation and production of interleukin-1 family members and play crucial roles in host defense against pathogens. However, dysregulated activation of inflammasomes is associated with intense inflammation, leading to the development of inflammatory diseases. Therefore, inflammasomes must be activated at a proper strength to protect against infection and avoid tissue damage. Recent studies have highlighted the cross-talk between inflammasome activation and autophagy, the cellular machinery associated with the degradation of intracellular components and maintenance of cellular homeostasis. Notably, deficiencies in autophagy-related proteins induce the aberrant activation of inflammasomes, causing severe tissue damage. In contrast, autophagy inducers ameliorate symptoms of inflammasome-related diseases. In this review, we discuss recent advances in the involvement of autophagy in regulating inflammasomes activation and in the development of inflammatory diseases.

Keywords: cytokines; endotoxin shock; inflammation; inflammatory bowel disease; signaling proteins; toll-like receptors/pattern recognition receptors.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy / genetics
  • Autophagy-Related Proteins / genetics
  • Bacterial Infections / immunology*
  • Crohn Disease / immunology*
  • Homeostasis
  • Humans
  • Immunity
  • Inflammasomes / metabolism*
  • Inflammation / immunology*
  • Interleukin-1 / metabolism*
  • RNA-Binding Proteins / metabolism


  • ATG16L1 protein, human
  • Autophagy-Related Proteins
  • Inflammasomes
  • Interleukin-1
  • P62 protein, human
  • RNA-Binding Proteins