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首页> 美国卫生研究院文献>Journal of Innate Immunity >Differential Regulation by Toll-Like Receptor Agonists Reveals That MCPIP1 Is the Potent Regulator of Innate Immunity in Bacterial and Viral Infections
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Differential Regulation by Toll-Like Receptor Agonists Reveals That MCPIP1 Is the Potent Regulator of Innate Immunity in Bacterial and Viral Infections

机译：类似收费受体激动剂的差异调节揭示了MCPIP1是细菌和病毒感染中固有免疫力的有效调节剂。

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Toll-like receptors (TLRs) are key molecules in innate immunity that recognize a variety of pathogen-associated molecular patterns. Activation of TLRs by their agonists initiates several signaling cascades, which eventually result in the expression of immune modifiers. Despite the fact that MCPIP1 is reported as an important immune regulator involved in macrophage activation, modulation of its expression by all known TLR agonists has never been documented. In this study, we present for the first time that in human monocyte-derived macrophages all TLR agonists, except CpG, markedly induced the expression of MCPIP1. The level of the induced transcript, as well as the protein and time of their appearance varied depending on the agonist. Furthermore, we confirmed the strong and differential upregulation of during bacteria, virus and fungus infection. belongs to a group of early-response genes; however, in the present study, we show for the first time the sustained high level of expression during long-term infection. Taken together, our results implicate as a potent regulator of innate immunity, which can be strongly engaged in the pathogenesis of acute and chronic infective diseases.
机译：Toll样受体（TLR）是先天免疫力中的关键分子，可识别多种病原体相关的分子模式。 TLR被其激动剂激活会引发多个信号级联反应，最终导致免疫修饰剂的表达。尽管据报道MCPIP1是参与巨噬细胞激活的重要免疫调节剂，但尚未见到所有已知TLR激动剂对其表达的调节。在这项研究中，我们首次提出在人类单核细胞衍生的巨噬细胞中，除CpG外，所有TLR激动剂均能明显诱导MCPIP1的表达。诱导的转录物的水平以及其出现的蛋白质和时间取决于激动剂。此外，我们确认了细菌，病毒和真菌感染期间的强而有差异的上调。属于一组早期反应基因；然而，在本研究中，我们首次显示了长期感染过程中持续高水平的表达。两者合计，我们的结果暗示作为先天免疫的有效调节剂，其可以强烈参与急性和慢性传染病的发病机理。

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