IFN-gamma-inducible Irga6 mediates host resistance against Chlamydia trachomatis via autophagy.
Ontology highlight
ABSTRACT: Chlamydial infection of the host cell induces Gamma interferon (IFNgamma), a central immunoprotector for humans and mice. The primary defense against Chlamydia infection in the mouse involves the IFNgamma-inducible family of IRG proteins; however, the precise mechanisms mediating the pathogen's elimination are unknown. In this study, we identify Irga6 as an important resistance factor against C. trachomatis, but not C. muridarum, infection in IFNgamma-stimulated mouse embryonic fibroblasts (MEFs). We show that Irga6, Irgd, Irgm2 and Irgm3 accumulate at bacterial inclusions in MEFs upon stimulation with IFNgamma, whereas Irgb6 colocalized in the presence or absence of the cytokine. This accumulation triggers a rerouting of bacterial inclusions to autophagosomes that subsequently fuse to lys
SUBMITTER: Al-Zeer MA
PROVIDER: S-EPMC2643846 | biostudies-literature | 2009
REPOSITORIES: biostudies-literature
ACCESS DATA