Toxoplasma TgIST co-opts Host Chromatin Repressors dampening STAT1-dependent gene regulation and IFN-γ-mediated host defenses

ABSTRACT: An early hallmark of Toxoplasma infection is the rapid control of the parasite population by a potent multifaceted innate immune response that engages resident and homing immune cells along with pro- and counter-inflammatory cytokines. In this context, IFN-γ activates a variety of Toxoplasma-targeting activities in immune and non-immune cells, but can also contribute to host immune pathology. Toxoplasma has evolved mechanisms to timely counteract the host IFN-γ defenses by interfering with the transcription of IFN-γ-stimulated genes. We now have identified TgIST as a critical molecular switch that is secreted by intracellular parasites and traffics to the host cell nucleus where it inhibits STAT1-dependent proinflammatory gene expression. We show that TgIST not only sequesters STAT1 on

ORGANISM(S): Homo sapiens

SUBMITTER: Mohamed-ali HAKIMI 

PROVIDER: E-GEOD-81613 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress