Figure 1.

Optimizing autophagy-mediated regulation of intracellular Mtb survival. At very low autophagy levels (shaded zone), cellular survival is compromised, killing Mtb collaterally. With an increase in autophagy flux (green line) cellular survival is maintained. When autophagy flux is coupled with xenophagy flux (red dotted line, as in the case of rapamycin treatment), bacterial survival again gets compromised. An interesting facet of this model is at the junction where an increase in autophagy flux rescues cell death. At this junction, an increase in autophagy could have probacterial effects rather than the established antibacterial function as long as the bacteria have a means of avoiding sequestration or (in the case of Mtb) maturation of bacteria-containing autophagosomes. The red inhibition mark highlights the point that Mtb selectively inhibits xenophagy flux.