Autophagy as an immune effector against tuberculosis. Academic Article Review uri icon

start page

  • 355

end page

  • 365


  • The now well-accepted innate immunity paradigm that autophagy acts as a cell-autonomous defense against intracellular bacteria has its key origins in studies with Mycobacterium tuberculosis, an important human pathogen and a model microorganism infecting macrophages. A number of different factors have been identified that play into the anti-mycobacterial functions of autophagy, and recent in vivo studies in the mouse model of tuberculosis have uncovered additional anti-inflammatory and tissue-sparing functions of autophagy. Complementing these observations, genome wide association studies indicate a considerable overlap between autophagy, human susceptibility to mycobacterial infections and predisposition loci for inflammatory bowel disease. Finally, recent studies show that autophagy is an important regulator and effector of IL-1 responses, and that autophagy intersects with type I interferon pathology-modulating responses.Copyright © 2013 Elsevier Ltd. All rights reserved.

date/time value

  • 2013

Digital Object Identifier (DOI)

  • 10.1016/j.mib.2013.05.003

PubMed Identifier

  • 23790398


  • 16


  • 3


  • Animals
  • Autophagy
  • Disease Models, Animal
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate
  • Mice
  • Mycobacterium tuberculosis
  • Tuberculosis