Journal
AUTOPHAGY
Volume 7, Issue 3, Pages 304-309Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.7.3.14539
Keywords
autophagy; innate immunity; ubiquitin; NDP52; p62; TBK1
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Funding
- MRC [MC_U105170648] Funding Source: UKRI
- Medical Research Council [MC_U105170648] Funding Source: researchfish
- Medical Research Council [MC_U105170648] Funding Source: Medline
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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.
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