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首页> 外文期刊>Infection and immunity >Macrophage Migration Inhibitory Factor Plays a Critical Role in Mediating Protection against the Helminth Parasite Taenia crassiceps
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Macrophage Migration Inhibitory Factor Plays a Critical Role in Mediating Protection against the Helminth Parasite Taenia crassiceps

机译：巨噬细胞迁移抑制因子在介导对蠕虫寄生虫Ta虫Ta虫的保护中起关键作用

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摘要

To determine the role of endogenous migration inhibitory factor (MIF) in regulation of immune response during murine cysticercosis caused by the helminth parasite Taenia crassiceps, we analyzed the course of T. crassiceps infection in MIF?/? BALB/c mice. MIF?/? mice were highly susceptible to T. crassiceps and developed significantly higher parasite loads compared to similarly infected MIF+/+ mice. Throughout the course of infection, Taenia crassiceps soluble antigen-stimulated spleen cells from both MIF+/+ and MIF?/? mice produced significant and comparable levels of interleukin-4 (IL-4), but those from MIF?/? mice produced significantly more IL-13, as well as gamma interferon (IFN-γ), suggesting that the susceptibility of MIF?/? mice to T. crassiceps was not due to the lack of IFN-γ production. Interestingly, low levels of both total and specific immunoglobulin G2a were observed in MIF?/? cysticercotic mice despite the high IFN-γ levels; in addition, peritoneal macrophages obtained from T. crassiceps-infected MIF?/? mice at different time points failed to respond efficiently to stimulation in vitro with lipopolysaccharide plus IFN-γ and produced significantly lower levels of IL-12, tumor necrosis factor alpha, and NO compared to those from MIF+/+ mice. These findings demonstrate that MIF plays a critical role in mediating protection against T. crassiceps in vivo. Moreover, these findings also suggest that impaired macrophage function rather than the lack of Th1 development may be responsible for mediating susceptibility to T. crassiceps.
机译：为了确定内源性迁移抑制因子（MIF）在蠕虫<虫Ta虫引起的小鼠囊尾ice病免疫调节中的作用，我们分析了 T的过程。 MIF ？/？ BALB / c小鼠中出现了狂犬病。 MIF ？/？小鼠对 T高度敏感。与类似感染的MIF + / + 小鼠相比，它们具有更大的寄生虫负荷。在整个感染过程中，MIF + / + 和MIF ？/？小鼠的 Taenia crassiceps 可溶性抗原刺激的脾细胞产生了明显的白细胞介素4（IL-4）的水平相当，但是MIF α/β小鼠的水平产生的IL-13以及γ-干扰素（IFN-γ）明显更多，这表明MIF ？/？小鼠到 T。并非由于缺乏IFN-γ产生。有趣的是，尽管IFN-γ水平高，但在MIF ？/？囊尾rc病小鼠中观察到的总免疫球蛋白G2a和特异性免疫球蛋白G2a的水平都较低。另外，从 T获得腹膜巨噬细胞。在不同的时间点，被狂犬病感染的MIF ？/？小鼠未能对脂多糖加IFN-γ的体外刺激产生有效的反应，并显着降低了IL-12，肿瘤坏死因子的水平α和NO与MIF + / + 小鼠相比。这些发现表明，MIF在介导针对 T的保护中起着关键作用。体内发生的狂犬病。此外，这些发现还表明，巨噬细胞功能受损而不是缺乏Th1发育可能是介导 T易感性的原因。狂犬病。

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