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. 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 phagocytosis (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. 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.

中文翻译：

---

自噬在寄生虫感染的控制和发病机制中。

自噬在防御寄生虫方面起着至关重要的作用。由于宿主细胞和微生物的种类，宿主自噬和寄生虫之间存在的相互作用具有不同的结果。自噬区室的存在破坏了大量病原体，并被自溶酶体中的异体吞噬进一步清除。另一部分病原体有能力以自己的优势战胜自噬途径。为了理解病原体和宿主细胞之间的相互作用，区分饥饿诱导的自噬和其他自噬途径具有重要意义。寄生虫对宿主自噬的破坏可能是由于细胞途径与“经典”自噬的差异，并且它们以一种特殊的方式受到寄生虫的控制。在细胞内水平的异食清除中，在自噬受体确认之前，病原体首先被泛素化，然后用轻链 3 (LC3) 蛋白标记。LC3 相关吞噬作用 (LAP) 中的 LC3 直接添加到液泡膜中，并且无论 ULK（一种起始复合物）如何发挥作用。由 ATG13、FIP200 和 ATG101 组成的 ULK 复合物的激活导致宿主自噬反应的启动。同样，保守的 PRR 对 PAMP 的识别标志着抵御病原体的第一道防线，包括 Toll 样受体 (TLR)。最近有报道称，这些所有重要的免疫相关受体都可以调节自噬。在这篇综述中，我们总结了自噬的最新进展，以认识和理解宿主和寄生虫之间的相互作用，重点关注用于治疗药物设计的靶蛋白。