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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >RELMbeta/FIZZ2 is a goblet cell-specific immune-effector molecule in the gastrointestinal tract.
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RELMbeta/FIZZ2 is a goblet cell-specific immune-effector molecule in the gastrointestinal tract.

机译：RELMbeta / FIZZ2是胃肠道中的杯状细胞特异性免疫效应分子。

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Gastrointestinal (GI) nematode infections are an important public health and economic concern. Experimental studies have shown that resistance to infection requires CD4(+) T helper type 2 (Th2) cytokine responses characterized by the production of IL-4 and IL-13. However, despite >30 years of research, it is unclear how the immune system mediates the expulsion of worms from the GI tract. Here, we demonstrate that a recently described intestinal goblet cell-specific protein, RELMbeta/FIZZ2, is induced after exposure to three phylogenetically distinct GI nematode pathogens. Maximal expression of RELMbeta was coincident with the production of Th2 cytokines and host protective immunity, whereas production of the Th1 cytokine, IFN-gamma, inhibited RELMbeta expression and led to chronic infection. Furthermore, whereas induction of RELMbeta was equivalent in nematode-infected wild-type and IL-4-deficient mice, IL-4 receptor-deficient mice showed minimal RELMbeta induction and developed persistent infections, demonstrating a direct role for IL-13 in optimal expression of RELMbeta. Finally, we show that RELMbeta binds to components of the nematode chemosensory apparatus and inhibits chemotaxic function of a parasitic nematode in vitro. Together, these results suggest that intestinal goblet cell-derived RELMbeta may be a novel Th2 cytokine-induced immune-effector molecule in resistance to GI nematode infection.
机译：胃肠道（GI）线虫感染是重要的公共卫生和经济问题。实验研究表明，对感染的抗性需要以产生IL-4和IL-13为特征的CD4（+）T辅助2型（Th2）细胞因子反应。然而，尽管进行了30多年的研究，但尚不清楚免疫系统如何介导蠕虫从胃肠道排出。在这里，我们证明了最近描述的肠道杯状细胞特异性蛋白RELMbeta / FIZZ2在暴露于三种系统发育不同的GI线虫病原体后被诱导。 RELMbeta的最大表达与Th2细胞因子的产生和宿主保护性免疫同时发生，而Th1细胞因子IFN-γ的产生抑制RELMbeta的表达并导致慢性感染。此外，虽然RELMbeta的诱导在线虫感染的野生型和IL-4缺陷的小鼠中是等效的，但IL-4受体缺陷的小鼠显示最小的RELMbeta诱导并发展为持续感染，证明IL-13在最佳表达中具有直接作用。 RELMbeta。最后，我们显示RELMbeta绑定到线虫化学感应仪器的组件，并在体外抑制寄生线虫的化学趋化功能。总之，这些结果表明，肠杯状细胞来源的RELMbeta可能是一种新型的Th2细胞因子诱导的针对胃肠道线虫感染的免疫效应分子。

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