Abstract:
Background: Autophagy has a crucial role in the defense against parasites. The interplay existing between host
autophagy and parasites has varied outcomes due to the kind of host cell and microorganism. The presence of
autophagic compartments disrupt a significant number of pathogens and are further cleared by xenophagy in an
autolysosome. Another section of pathogens have the capacity to outwit the autophagic pathway to their own
advantage.
Result: To comprehend the interaction between pathogens and the host cells, it is significant to distinguish between
starvation-induced autophagy and other autophagic pathways. Subversion of host autophagy by parasites is likely
due to differences in cellular pathways from those of ‘classical’ autophagy and that they are controlled by parasites in a
peculiar way. In xenophagy clearance at the intracellular level, the pathogens are first ubiquitinated before autophagy
receptors acknowledgement, followed by labeling with light chain 3 (LC3) protein. The LC3 in LC3-associated phago‑
cytosis (LAP) is added directly into vacuole membrane and functions regardless of the ULK, an initiation complex.
The activation of the ULK complex composed of ATG13, FIP200 and ATG101causes the initiation of host autophagic
response. Again, the recognition of PAMPs by conserved PRRs marks the first line of defense against pathogens,
involving Toll-like receptors (TLRs). These all important immune-related receptors have been reported recently to
regulate autophagy.
Conclusion: In this review, we sum up recent advances in autophagy to acknowledge and understand the interplay
between host and parasites, focusing on target proteins for the design of therapeutic drugs. The target host proteins
on the initiation of the ULK complex and PRRs-mediated recognition of PAMPs may provide strong potential for the
design of therapeutic drugs against parasitic infections.
