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首页> 外文期刊>Microbes and infection >Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-gamma-induced major histocompatibility complex class II gene expression
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Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-gamma-induced major histocompatibility complex class II gene expression

机译：弓形虫利用多种机制抑制IFN-γ诱导的主要组织相容性复合物II类基因表达

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The intracellular parasite Toxoplasma gondii is able to establish persistent infections in immunocompetent hosts and this may be facilitated by different immune evasion mechanisms. In the present study, we describe that infection of marine monocyte/macrophage RAW 264.7 cells with T. gondii blocks the IFN-gamma-induced upregulation of major histocompatibility complex (MHC) class II mRNAs and proteins. Heat inactivation of the parasites prior to host cell invasion, but not inhibition of the intracellular replication of T. gondii abolished the inhibition of MHC class II upregulation. Interestingly, a T. gondii lysate (TL) mimicked the inhibitory effect of viable parasites on MHC class II expression. Nuclear translocation of the signal transducer and activator of transcription in response to IFN-gamma were normal both in cells incubated with TL or infected with viable parasites. Transcript levels of the class II transactivator and consequently H2-Ab were nevertheless diminished by both viable parasites and TL. In contrast, interferon regulatory factor-1 mRNA was only decreased in response to viable T. gondii. Luciferase reporter assays confirmed differential effects of viable parasites and TL on minimal or complex IFN-gamma-responsive promoters. Furthermore, only TL, and not viable parasites, strongly induced the secretion of IL-10 by marine macrophages. Whereas TL also inhibited MHC class II expression in macrophages from IL-10-deficient mice, increased IL-10 secretion by wild type macrophages did not mediate the block in MHC class II upregulation. In conclusion, T. gondii employs different mechanisms to inhibit MHC class II expression, suggesting a complex regulation of this immune evasion strategy. (c) 2006 Elsevier SAS. All rights reserved.
机译：细胞内的寄生虫弓形虫能够在具有免疫能力的宿主中建立持续性感染，并且可以通过不同的免疫逃逸机制来促进。在本研究中，我们描述了用弓形虫感染海洋单核细胞/巨噬细胞RAW 264.7细胞可阻断IFN-γ诱导的主要组织相容性复合物（MHC）II类mRNA和蛋白的上调。在宿主细胞入侵之前将寄生虫加热灭活，但不能抑制弓形虫的细胞内复制，从而消除了对MHC II类上调的抑制作用。有趣的是，刚地弓形虫的裂解物（TL）模仿了活寄生虫对MHC II类表达的抑制作用。在与TL孵育或感染了活寄生虫的细胞中，响应IFN-γ的信号转导子和转录激活子的核易位均正常。然而，II类反式激活因子和H2-Ab的转录水平却被寄生虫和TL降低了。相比之下，干扰素调节因子-1 mRNA仅在响应弓形虫后才降低。萤光素酶报告基因测定证实了活的寄生虫和TL对最小或复杂的IFN-γ反应启动子的不同作用。此外，只有TL，而不是活的寄生虫，强烈诱导了海洋巨噬细胞分泌IL-10。 TL还抑制了IL-10缺陷小鼠巨噬细胞中MHC II类的表达，而野生型巨噬细胞分泌的IL-10增加并未介导MHC II类上调的阻滞。总之，弓形虫采用不同的机制抑制II类MHC表达，表明该免疫逃避策略的复杂调控。 （c）2006年Elsevier SAS。版权所有。

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