Toxoplasma gondii effector TgIST blocks type I interferon signaling to promote infection.

ABSTRACT: In contrast to the importance of type II interferon-γ (IFN-γ) in control of toxoplasmosis, the role of type I IFN is less clear. We demonstrate here that TgIST, a secreted effector previously implicated in blocking type II IFN-γ signaling, also blocked IFN-β responses by inhibiting STAT1/STAT2-mediated transcription in infected cells. Consistent with a role for type I IFN in cell intrinsic control, ∆Tgist mutants were more susceptible to growth inhibition by murine and human macrophages activated with IFN-β. Additionally, type I IFN was important for production of IFN-γ by natural killer (NK) cells and recruitment of inflammatory monocytes at the site of infection. Mice lacking type I IFN receptors (Ifnar1^-/-) showed increased mortality following infection with wild-type

SUBMITTER: Matta SK 

PROVIDER: S-EPMC6717281 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature