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- W4210604472 abstract "Toxoplasma gondii is an opportunistic protozoan, which widely infects humans and other warm-blooded animals. The type I interferon (IFN) such as IFN-α/β is involved in cGAS-STING signaling to resist T. gondii infection. We found in RAW264.7 cells, that T. gondii virulence factor TgROP18I , inhibited IFN-β production through interacting with interferon regulatory factor 3 (IRF3). Besides, TgROP18I interacted with p62 and Tumor Necrotic Factor Receptor Associated Factor 6 (TRAF6), which resulted in the inhibition of TRAF6-p62 interaction, and phosphorylation of p62. Furthermore, TgROP18I restricted the recruitment of ubiquitin, p62 and microtubule-associated protein light chain 3 (LC3) to the parasitophorous vacuole membrane (PVM) in IFN-γ-stimulated murine cell line L929 cells. In IFN-γ-stimulated human cells, TgROP18I restricted the decoration of PVM with ubiquitin, p62, and LC3, and bound with TRAF2, TRAF6, and p62, respectively. As a result, TgROP18I led to a successful parasitic replication in murine and human cells. Collectively, our study revealed the function of TgROP18I in suppressing host type I interferon responses in T. gondii infection for parasitic immune escape." @default.
- W4210604472 created "2022-02-08" @default.
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- W4210604472 date "2022-01-27" @default.
- W4210604472 modified "2023-10-11" @default.
- W4210604472 title "<i>Toxoplasma gondii</i>ROP18<sub>I</sub>inhibits host innate immunity through cGAS‐STING signaling" @default.
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- W4210604472 doi "https://doi.org/10.1096/fj.202101347r" @default.
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