弓形虫抑制γ干扰素依赖的宿主细胞免疫的研究进展

摘要/Abstract

摘要：

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。

关键词: 刚地弓形虫, IFN-γ, 细胞免疫, 免疫逃避, 泛素蛋白

Abstract:

It has been reported that Toxoplasma gondii, after invading mouse cells, secrets a virulence factor ROP18 to bind and phosphorylate immunity-related p47 GTPase (IRG), inhibiting its binding to parasitophorous vacuole membrane (PVM) and thus the breakage of the parasitophorous vacuole (PV), enabling the growth and proliferation of T. gondii in the PVs. In contrast to the elucidation of immune escape mechanism of T. gondii in mouse cells, little is known in human cells. It is reported that the ubiquitin-labeled PVs can fuse with the lysosomal system in human cells, which results in death of T. gondii tachyzoits by acidification. This review summarizes the mechanisms by which T. gondii inhibits cellular immunity, especially the interferon-γ-dependent cellular immunity in host cells. In our understanding of immune evasion of T. gondii through blocking ubiquitination of PVs, recent advances are reviewed as well.

Key words: Toxoplasma gondii, Interferon-γ, Cellular immunity, Immune evasion, Ubiquitin

中图分类号:

R382.5

姚礼捷, 彭鸿娟. 弓形虫抑制γ干扰素依赖的宿主细胞免疫的研究进展[J]. 中国寄生虫学与寄生虫病杂志, 2017, 35(5): 503-508.

Li-jie YAO, Hong-juan PENG. Research advances on the inhibition of interferon-γ-dependent cellular immunity by Toxoplasma gondii[J]. Chinese Journal of Parasitology and Parasitic Diseases, 2017, 35(5): 503-508.

图/表 1

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