Autophagy and LAP in the Fight against Fungal Infections: Regulation and Therapeutics

Figure 2

Proposed model of cross-regulation between LAP and canonical autophagy in p47^phox−/− mice. The figure shows that both autophagy and LAP are defective in p47^phox−/− mice. Rapamycin, a known inducer of canonical autophagy, failed to promote fungal clearance and reduce inflammation when administered to CGD mice as opposed to IFN-γ that promoted fungal clearance and reduced pathogenic inflammation by inducing the LAP/DAPK1 pathway. Thus, canonical autophagy and LAP are distinct pathways in Aspergillus infection, and LAP, more than canonical autophagy, is required for optimal antifungal resistance. CGD: chronic granulomatous disease; DAPK1: death-associated protein kinase 1; IFN-γ: interferon gamma; LAP: LC3-associated phagocytosis; WT: wild type.