IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.

IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.
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IFI16 通过促进 HTLV-1 RTI 诱导的先天免疫反应来调节 HTLV-1 复制。

DOI:
10.1002/1873-3468.13077
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发表时间:
2018
期刊:
影响因子:
3.5
通讯作者:
Wang Jie
Wang Jie
中科院分区:
生物学3区
文献类型:
--
作者:
Yang Bo;Song Di;Liu Yue;Cui Yuhan;Lu Guangjian;Di Wenyu;Xing Hongxia;Ma Lingling;Guo Zhixiang;Guan Yuhe;Wang Hui;Wang Jie

文献摘要

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干扰素(IFN)诱导蛋白16(IFI 16)作为DNA传感器通过诱导先天性免疫应答调节人类免疫缺陷病毒复制。人类嗜T淋巴细胞病毒1型(HTLV-1)是一种δ逆转录病毒家族成员,与多种疾病有关。在这里,我们报告了IFI 16表达是由HTLV-1感染或HTLV-1逆转录中间体(RTI)ssDNA 90转染诱导的。IFI 16过表达降低HTLV-1蛋白表达,而IFI 16敲低则增加其表达。此外,IFI 16敲低后,HTLV-1感染后先天免疫应答受损。此外,IFI 16与ssDNA 90形成复合物并增强ssDNA 90触发的先天免疫应答。总的来说,我们的数据表明IFI 16在HTLV-1感染期间通过与HTLV-1 RTI ssDNA 90相互作用并限制HTLV-1复制而发挥关键作用。
Interferon (IFN)‐inducible protein 16 (IFI16) regulates human immunodeficiency virus replication by inducing innate immune responses as a DNA sensor. Human T‐lymphotropic virus type 1 (HTLV‐1), a delta retrovirus family member, has been linked to multiple diseases. Here, we report that IFI16 expression is induced by HTLV‐1 infection or HTLV‐1 reverse transcription intermediate (RTI) ssDNA90 transfection. IFI16 overexpression decreases HTLV‐1 protein expression, whereas IFI16 knockdown increases it. Furthermore, the knockdown of IFI16 is followed by impaired innate immune responses upon HTLV‐1 infection. In addition, IFI16 forms a complex with ssDNA90 and enhances ssDNA90‐triggered innate immune responses. Collectively, our data suggest a critical role for IFI16 during HTLV‐1 infection by interacting with HTLV‐1 RTI ssDNA90 and restricting HTLV‐1 replication.