LAP requires some conventional autophagy-related proteins, such as LC3, Beclin-1, Rubicon, etc.
22,33 Compared with canonical autophagy, pre-initiation complex activity is not necessary for LAP, but it requires the class III PI3K complex.
7 The class III PI3K complex member Beclin-1 is recruited to the phagosomes almost instantly.
34 Rubicon, a class III PI3K related protein that interacts with Beclin-1, has also been shown to be essential for the stable anchoring of LC3-II on LAP.
35 Furthermore, previous studies have found that the autophagy protein ATG-7 is crucial for LAP. The absence of ATG-7 results in a reduction in the recruitment of LC3-II, which makes phagocytosis less effective in killing and eliminating apoptotic cells.
16 LC3-II is localized on the monolayer membrane of phagocytic vesicles, facilitating the maturation of single-membrane phagosomes, their fusion with lysosomes, the clearance of ingested pathogens, and enhancing the efficacy of fungal elimination.
17,34 Our results demonstrated that the expression of LAP-related proteins was significantly elevated in
A. fumigatus-infected human and mouse corneas. Moreover, the formation of positive GFP-LC3 puncta was notably enhanced in mice corneas with FK. The above results revealed that LAP may have a potential role in
A. fumigatus keratitis. Recent research has indicated that LAP was rapidly formed when RAW 264.7 cells phagocytosed zymosan, LPS, and
Escherichia coli.36 Consistently, stimulation with LPS upregulates the expression of LAP-associated proteins, thereby promoting the facilitation of pathogen elimination. This reminded us that LAP could play a role in the elimination of invading fungal pathogens in
A. fumigatus keratitis. The above evidence indicated that LAP was involved in the immune process of
A. fumigatus keratitis.