MicroRNA-155 (miRNA-155) is known to play an important role in the regulation of innate and adaptive immune responses in mammals. However, no information is available on the role of miRNA-155 in relation to type I interferon (IFN) responses in fish cells. In the present study, we found that the protein inhibitor of activated STAT 4a (PIAS4a) gene of fathead minnow (Pimephales promelas) was a target of miR-155, which was verified by the inhibitory activity of miR-155 in the expression of reporter gene harboring 3′UTR of PIAS4a of EPC cells. Furthermore, cells over-expressing miR-155 showed a significantly higher type I IFN response after polyinosinic-polycytidylic acid (poly I:C) stimulation, suggesting the targeting of PIAS4a in EPC cells by miR-155 can be a cause of the up-regulation of type I IFN, and miR-155 can act as an antiviral factor. However, as the targeting PIAS4a might not be the sole cause of the type I IFN up-regulation by miR-155, further studies on the uncovering of miR-155 target genes that are involved in type I IFN responses in fish are required.

已知MicroRNA-155（miRNA-155）在调节哺乳动物的先天和适应性免疫应答中起重要作用。但是，尚无关于miRNA-155与鱼细胞中I型干扰素（IFN）反应相关的信息。在本研究中，我们发现了黑头呆fat（Pimephales promelas）的活化STAT 4a（PIAS4a）基因的蛋白抑制剂）是miR-155的靶标，这已通过miR-155对EPC细胞PIAS4a 3'UTR的报告基因表达的抑制活性而得到证实。此外，过度表达miR-155的细胞在多肌苷酸-聚胞苷酸（poly I：C）刺激后显示出显着更高的I型IFN反应，这表明miR-155对EPC细胞中PIAS4a的靶向作用可能是引起I-IFN升高的原因。调节I型IFN和miR-155可以作为抗病毒因子。但是，由于靶向PIAS4a可能不是miR-155引起I型IFN上调的唯一原因，因此需要进一步研究发现鱼类中涉及I型IFN反应的miR-155靶基因。