Zhaoxia Zhang, Haorong Gu, Qi Li, Jun Zheng, Shinuo Cao, Changjiang Weng, Honglin Jia

Infect Immun. 2020 Feb 24. pii: IAI.00054-20. doi: 10.1128/IAI.00054-20

Abstract

IFN-γ-induced innate immune responses play important roles in the inhibition of Toxoplasma gondii infection. It was reported that IFN-γà stimulates non-acidification-dependent growth restriction of T. gondii in HeLa cells, but the mechanism remains unclear. Here, we found that γ-aminobutyric acid (GABA) receptor-associated protein-like 2 (GABARAPL2) plays a critical role in parasite restriction in IFN-γ-treated HeLa cells, and LC3b do not have the overlapped function. 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-γ-induced immune response. These findings provide further understanding of a noncanonical autophagy pathway responsible for IFN-γ-dependent inhibition of T. gondii growth in human HeLa cells and demonstrate the critical role of GABARAPL2 in this response.

Copyright © 2020 American Society for Microbiology.