GABARAPL2 Is Critical for Growth Restriction of Toxoplasma gondii in HeLa Cells Treated with Gamma Interferon.

ABSTRACT: Gamma interferon (IFN-?)-induced innate immune responses play important roles in the inhibition of Toxoplasma gondii infection. It has been reported that IFN-? stimulates non-acidification-dependent growth restriction of T. gondii in HeLa cells, but the mechanism remains unclear. Here, we found that ?-aminobutyric acid (GABA) receptor-associated protein-like 2 (GABARAPL2) plays a critical role in parasite restriction in IFN-?-treated HeLa cells. GABARAPL2 is recruited to membrane structures surrounding parasitophorous vacuoles (PV). Autophagy adaptors are required for the proper localization and function of GABARAPL2 in the IFN-? -induced immune response. These findings provide further understanding of a noncanonical autophagy pathway responsible for IFN-?-dependent inhibition of T. gondii growth in human HeLa cells and demonstrate the critical role of GABARAPL2 in this response.

SUBMITTER: Zhang Z 

PROVIDER: S-EPMC7171250 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature