CHINESE JOURNAL OF PARASITOLOGY AND PARASITIC DISEASES ›› 2017, Vol. 35 ›› Issue (5): 503-508.

• Orginal Article • Previous Articles     Next Articles

Research advances on the inhibition of interferon-γ-dependent cellular immunity by Toxoplasma gondii

Li-jie YAO, Hong-juan PENG*()   

  1. Department of Pathogen Biology, Guangdong Provincial Key Laboratory of Tropical Disease Research, Southern Medical University, Guangzhou, 510515, China
  • Received:2017-04-05 Online:2017-10-30 Published:2018-01-08
  • Contact: Hong-juan PENG E-mail:hongjuan@smu.edu.cn
  • Supported by:
    Supported by the National Natural Science Foundation of China (No. 81572012,81772217), the National Key Research and Development Program of China (No. 2017YFD0500400), Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (2014), Guangdong Provincial Natural Science Fund Key Project (No. 2016A030311025), and Guangzhou Health and Medical Collaborative Innovation Major Special Project(No. 201604020011)

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

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