How cells deploy ubiquitin and autophagy to defend their cytosol from bacterial invasion

Autophagy. 2011 Mar;7(3):304-9. doi: 10.4161/auto.7.3.14539.


Autophagy serves as a cell-autonomous effector mechanism of innate immunity in the cytosol. Autophagy restricts bacterial proliferation by separating bacteria from the nutrient-rich cytosol and delivering them into bactericidal autolysosomes. Autophagy also restricts inflammation by enclosing the membrane remnants of vacuoles from which bacteria have escaped. In contrast to starvation-induced autophagy, which engulfs cytosol nonspecifically, antibacterial autophagy is receptor-mediated and selective. Several distinct pathways of antibacterial autophagy have been identified recently, which can be triggered by either bacterial PAMPs, host-mediated modifications of bacteria-containing vacuoles, or cytosolic bacteria that have become decorated with ubiquitin. Ubiquitin-coated bacteria are sensed by p62, a promiscuous autophagy receptor required for the uptake of a variety of ubiquitin-marked autophagy substrates, and by NDP52, an autophagy receptor that, by associating with the immunoregulatory kinase TBK1, may serve a dedicated function in cytosolic immunity.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / chemistry
  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Autophagy*
  • Bacteria / metabolism*
  • Cytosol / immunology
  • Cytosol / microbiology*
  • Humans
  • Models, Biological
  • Ubiquitin / metabolism*


  • Adaptor Proteins, Signal Transducing
  • Ubiquitin