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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Activation of innate immune defense mechanisms by signaling through RIG-I/IPS-1 in intestinal epithelial cells.
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Activation of innate immune defense mechanisms by signaling through RIG-I/IPS-1 in intestinal epithelial cells.

机译：通过在肠上皮细胞中通过RIG-I / IPS-1进行信号传导来激活先天性免疫防御机制。

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摘要

Intestinal epithelial cells (IECs) are a first line of defense against microbial pathogens that enter the host through the intestinal tract. Moreover, viral pathogens that infect the host via the intestinal epithelium are an important cause of morbidity and mortality. However, the mechanisms by which viral pathogens activate antiviral defense mechanisms in IECs are largely unknown. The synthetic dsRNA analog polyinosinic-polycytidylic acid and infection with live virus were used to probe the molecules that are activated and the mechanisms of signaling in virus-infected human IECs. Polyinosinic-polycytidylic acid activated IFN regulatory factor 3 dimerization and phosphorylation, increased activity of the IFN-stimulated response element, induced a significant increase in IFN-beta mRNA transcripts and IFN-beta secretion, and up-regulated the expression of IFN-regulated genes in IECs. Those responses were dependent upon activation of the dsRNA binding protein retinoic acid inducible gene I (RIG-I) and theRIG-I interacting protein IFN promoter stimulator-1, but not on dsRNA-activated protein kinase or TLR3, which also were expressed by IECs. Virus replication and virus-induced cell death increased in IECs in which RIG-I was silenced, consistent with the importance of the RIG-I signaling pathway in IEC antiviral innate immune defense mechanisms.
机译：肠道上皮细胞（IEC）是抵御微生物病原体通过肠道进入宿主的第一道防线。此外，通过肠上皮感染宿主的病毒病原体是发病和死亡的重要原因。但是，在IEC中，病毒病原体激活抗病毒防御机制的机制尚不清楚。合成的dsRNA类似物聚肌苷酸-聚胞苷酸和活病毒感染被用于探测被病毒感染的人类IEC中被激活的分子和信号传导机制。聚肌苷酸-聚胞苷酸激活了IFN调节因子3的二聚化和磷酸化，增强了IFN刺激的反应元件的活性，诱导IFN-beta mRNA转录和IFN-beta分泌显着增加，并上调了IFN调控基因的表达。在IEC中。这些反应取决于dsRNA结合蛋白视黄酸诱导基因I（RIG-1）和RIG-1相互作用蛋白IFN启动子stimulator-1的激活，而不取决于dsRNA激活的蛋白激酶或TLR3，后者也由IECs表达。在RIG-I被沉默的IEC中，病毒复制和病毒诱导的细胞死亡增加，这与RIG-I信号通路在IEC抗病毒先天免疫防御机制中的重要性相一致。

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