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近年来的研究表明,弓形虫感染小鼠细胞后,分泌的毒力蛋白——棒状体蛋白18(ROP18)能与免疫相关GTP酶(IRG)结合并使其发生磷酸化,致使IRG不能结合至纳虫泡膜上,纳虫泡不发生破裂,弓形虫得以在纳虫泡中生长增殖。此为弓形虫在小鼠细胞内实现免疫逃避的机制,但是弓形虫感染人细胞后的免疫逃避机制尚未明了。据报道,人细胞中泛素标记的纳虫泡能与内溶酶体系统融合,最终导致弓形虫因酸化而死亡。为此,本文综述了近年来弓形虫抑制宿主免疫功能,尤其是γ干扰素依赖的细胞免疫,以及弓形虫通过阻断泛素标记纳虫泡膜进而成功实现免疫逃避的研究进展。
In recent years, studies have shown that Toxoplasma gondii infection of mouse cells, secreted virulence protein - rod protein 18 (ROP18) with immune-related GTPase (IRG) and make it phosphorylated, resulting in IRG can not bind to On the mesophyll bubble membrane, the mesiozoite does not rupture, and the toxoplasma gondii grows and proliferates in the nanoblast bubble. Toxoplasma gondii in mice cells to achieve immune escape mechanism, but Toxoplasma gondii infection in human immune escape mechanism is not yet clear. It has been reported that ubiquitin-labeled nasal parasites in human cells fuse with the endolytic system, eventually leading to the death of Toxoplasma gondii due to acidification. Therefore, this review summarizes the recent progress of Toxoplasma gondii inhibiting host immune function, especially IFN-gamma-dependent cellular immunity, and Toxoplasma gondii succeeding in immune evasion by blocking the ubiquitin-labeled bubo.