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. 2018 May 23;9:935. doi: 10.3389/fimmu.2018.00935

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Copyright © 2018 Siqueira, Ribeiro and Travassos.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of autophagy induction by Salmonella Typhimurium. Upon entry in epithelial cells, S. Typhimurium resides in a specialized compartment, the Salmonella-containing vacuole (SCV). A fraction of the bacterial population damages and/or escapes from SCV and initiates to replicate in the cytosol. Either still within the SCV or free in the cytosolic compartment, S. Typhimurium triggers autophagy by several means. β-glycan present in vacuole remnants is recognized by Galectin-8 (Gal-8) and targets bacteria to autophagosomes. S. Typhimurium can also be ubiquitinated by the E3-ligases LRSAM or LUBAC, allowing its recognition by autophagic adaptors Optneurin, p62 or NDP52. RNF166, another E3-ligase, ubiquitinates p62 to increase the ability of this protein to bind bacteria-associated ubiquitin. Diacylglycerol (DAG) recognition and autophagy induction upon S. Typhimurium infection are not depicted here.