Autophagy regulates inflammatory responses in antigen-presenting cells: Underlying mechanisms

James Harris, Tali Lang, Maria B. Sukkar

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Otherpeer-review


Autophagy is a highly conserved homeostatic mechanism for the lysosomal degradation of cytosolic constituents, including proteins and organelles. Studies over the past 10 years have demonstrated a number of specific roles for autophagy in the regulation of host immune responses, host-microbe interactions, and inflammation. This chapter presents some of the known and proposed mechanisms through which autophagy impacts on inflammatory responses elicited by antigen-presenting cells, with a particular emphasis on the modulation of cytokine expression, production, and release. Through regulation of the IL-1 family cytokines, IL-1a, IL-1Β, and IL-18, autophagy has far-reaching impacts on numerous immune cell types, in particular by influencing the secretion of IL-23 and IL-17. Autophagy intersects with IL-1Β both directly, through sequestration of the cytokine in autophagosomes, and indirectly, through regulation of inflammasome activation in response to inflammatory stimuli. Perturbations in autophagic activity can also affect the secretion of other cytokines, including macrophage migration inhibitory factor. A better understanding of how autophagy exerts its effects on inflammation has the potential to open new therapeutic avenues for the treatment of diseases with inflammatory pathologies.

Original languageEnglish
Title of host publicationAutophagy
Subtitle of host publicationCancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging
EditorsM. A. Hayat
Place of PublicationLondon UK
PublisherAcademic Press
Number of pages17
ISBN (Electronic)9780128121474
ISBN (Print)9780128121467
Publication statusPublished - 2017


  • AIM2
  • ALRs
  • Inflammasome
  • Interleukin 1
  • MIF
  • NLRP3
  • NOD-like receptors

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