Suppr超能文献

细胞因子信号传导抑制因子1(SOCS1)在鲑鱼抗病毒免疫中的保守抑制作用。

A conserved inhibitory role of suppressor of cytokine signaling 1 (SOCS1) in salmon antiviral immunity.

作者信息

Sobhkhez Mehrdad, Joensen Lisbeth L, Tollersrud Linn Greiner, Strandskog Guro, Thim Hanna L, Jørgensen Jorunn B

机构信息

The Norwegian College of Fishery Science, UiT The Arctic University of Norway, N-9037 Tromsø, Norway.

The Norwegian College of Fishery Science, UiT The Arctic University of Norway, N-9037 Tromsø, Norway.

出版信息

Dev Comp Immunol. 2017 Feb;67:66-76. doi: 10.1016/j.dci.2016.11.001. Epub 2016 Nov 3.

Abstract

The SOCS proteins are regulators of JAK/STAT signaling. A number of viral infections has been associated with SOCS upregulation. Here we report that SOCS1 mRNA expression is up-regulated in salmon alphavirus (SAV3) infected TO cells, while infectious pancreatic necrosis virus infection has a negligible effect. SAV3 infected salmon showed increased SOCS1 mRNA levels in heart correlating with increased viral transcripts. Together, the in vitro and in vivo data suggests that SAV3-induced SOCS1 expression may affect the outcome of the virus infection. Using CHSE-214 cells overexpressing SOCS1 we revealed increased SAV3 replication compared to control, suggesting that SOCS1 suppress the antiviral capacity of the cells. In IFNa1-treated cells, the suppression of viral replication was partially rescued by SOCS1 overexpression. The increased viral replication in SOCS1 transgene cells was likely a result of impaired IFN-signaling and the reduced expression of interferon-stimulated genes in the transgene cells underscores this.

摘要

SOCS蛋白是JAK/STAT信号通路的调节因子。多种病毒感染与SOCS上调有关。在此我们报告,在感染鲑鱼α病毒(SAV3)的TO细胞中,SOCS1 mRNA表达上调,而感染传染性胰腺坏死病毒的影响可忽略不计。感染SAV3的鲑鱼心脏中SOCS1 mRNA水平升高,与病毒转录本增加相关。总之,体外和体内数据表明,SAV3诱导的SOCS1表达可能影响病毒感染的结果。使用过表达SOCS1的CHSE-214细胞,我们发现与对照相比SAV3复制增加,这表明SOCS1抑制细胞的抗病毒能力。在IFNa1处理的细胞中,SOCS1过表达部分挽救了病毒复制的抑制。SOCS1转基因细胞中病毒复制增加可能是IFN信号受损的结果,转基因细胞中干扰素刺激基因表达的降低强调了这一点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验