Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation.

Avian Leukosis Virus Subgroup J Attenuates Type I Interferon Production Through Blocking IκB Phosphorylation.
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禽白血病病毒 J 亚型通过阻断 I kappa B 磷酸化来减弱 I 型干扰素的产生

DOI:
10.3389/fmicb.2018.01089
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发表时间:
2018
影响因子:
5.2
通讯作者:
Xie Q
Xie Q
中科院分区:
生物学2区
文献类型:
--
作者:
Lin W;Xu Z;Yan Y;Zhang H;Li H;Chen W;Chen F;Xie Q

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J亚群禽白血病病毒(ALV-J)是一种致癌的逆转录病毒,可引起免疫抑制,增强继发感染的易感性,造成巨大的经济损失。虽然ALV-J诱导的免疫抑制已经被很好地建立,这种诱导的潜在分子机制仍然不清楚。在这里,我们报告ALV-J感染对I型干扰素表达的抑制作用与宿主细胞中转录调节因子NF-κB的下调有关。结果表明,ALV-J对HD 11细胞I型干扰素的产生具有抑制作用; ALV-J可上调IκBα的表达,下调NF-κ Bp 65的表达;总的来说,我们的研究结果提供了ALV-J的发病机制的见解。
Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection, resulting in great economic losses. Although ALV-J-induced immunosuppression has been well established, the underlying molecular mechanism for such induction is still unclear. Here, we report that the inhibitory effect of ALV-J infection on type I interferon expression is associated with the down-regulation of transcriptional regulator NF-κB in host cells. We found that ALV-J possess the inhibitory effect on type I interferon production in HD11 cells and that ALV-J causes the up-regulation of IκBα and down-regulation of NF-κB p65, and that ALV-J blocks the phosphorylation of IκBα on Ser32/36 amino acid residues. Collectively, our findings provide insights into the pathogenesis of ALV-J.
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