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首页> 外文期刊>Infection and immunity >Host Resistance and Immune Deviation in Pigeon Cytochromec T-Cell Receptor Transgenic Mice Infected withToxoplasma gondii
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Host Resistance and Immune Deviation in Pigeon Cytochromec T-Cell Receptor Transgenic Mice Infected withToxoplasma gondii

机译：刚体弓形虫感染的鸽子细胞色素T细胞受体转基因小鼠的宿主抗性和免疫变异

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Resistance to Toxoplasma gondii has been shown to be mediated by gamma interferon (IFN-γ) produced by NK, CD4+, and CD8+ T cells. While studies of SCID mice have implicated NK cells as the source of the cytokine in acute infection, several lines of evidence suggest that IFN-γ production by CD4+ T lymphocytes also plays an important role in controlling early parasite growth. To evaluate whether this function is due to nonspecific as opposed to T-cell receptor (TCR)-dependent stimulation by the parasite, we have examined the resistance toT. gondii infection of pigeon cytochrome ctransgenic (PCC-Tg) Rag-2?/? mice in which all CD4+ T lymphocytes are unreactive with the protozoan. When inoculated with the ME49 strain, PCC-Tg animals exhibited only temporary control of acute infection and succumbed by day 17. Intracellular cytokine staining by flow cytometry revealed that, in contrast to infected nontransgenic controls, infected PCC-Tg animals failed to develop IFN-γ-producing CD4+ T cells. Moreover, the CD4+ lymphocytes from these mice showed no evidence of activation as judged by lack of upregulated expression of CD44 or CD69. Nevertheless, when acutely infected transgenic mice were primed by PCC injection, the lymphokine responses measured after in vitro antigen restimulation displayed a strong Th1 bias which was shown to be dependent on endogenous interleukin 12 (IL-12). The above findings argue that, while T. gondii-induced IL-12 cannot trigger IFN-γ production by CD4+ T cells in the absence of TCR ligation, the pathogen is able to nonspecifically promote Th1 responses against nonparasite antigens, an effect that may explain the immunostimulatory properties of T. gondii infection.
机译：已显示对弓形虫的抗性由NK，CD4 +和CD8 + T细胞产生的γ干扰素（IFN-γ）介导。尽管对SCID小鼠的研究表明在急性感染中NK细胞是细胞因子的来源，但几条证据表明CD4 + T淋巴细胞产生的IFN-γ在控制早期寄生虫生长中也起着重要作用。为了评估该功能是否是由于非特异性的，而不是寄生虫的T细胞受体（TCR）依赖性刺激，我们检查了对T的抗性。鸽感染细胞色素C基因转基因（PCC-Tg）Rag-2α/β所有CD4 + T淋巴细胞均与原生动物无反应的小鼠。接种ME49株后，PCC-Tg动物仅表现出对急性感染的暂时控制，并在第17天死亡。流式细胞术对细胞内细胞因子染色显示，与感染的非转基因对照相比，感染的PCC-Tg动物未能产生IFN-γ产生γ的CD4 + T细胞。此外，这些小鼠的CD4 +淋巴细胞未显示出激活的迹象，而CD44或CD69的表达缺乏上调可以判断该激活。然而，当急性感染的转基因小鼠通过PCC注射引发时，在体外抗原再刺激后测得的淋巴因子反应显示出强烈的Th1偏倚，该偏倚显示出依赖于内源性白介素12（IL-12）。上述发现认为，尽管在没有TCR的情况下，弓形虫诱导的IL-12不能触发CD4 + T细胞产生IFN-γ，但病原体能够非特异性地促进针对非寄生虫抗原的Th1反应。弓形虫感染的免疫刺激特性。

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