Interferon-induced Transmembrane Protein 3 Prevents Acute Influenza Pathogenesis in Mice.

Interferon-induced Transmembrane Protein 3 Prevents Acute Influenza Pathogenesis in Mice.
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DOI:
10.3967/bes2020.041
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发表时间:
2020-05
期刊:
Biomedical and environmental sciences : BES
影响因子:
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通讯作者:
Qiang Sun;Na Lei;Jian Lu;R. Gao;Zi Li;Li Qi Liu;Ying Sun;Jun-feng Guo;Da Yan Wang;Y. Shu
Qiang Sun;Na Lei;Jian Lu;R. Gao;Zi Li;Li Qi Liu;Ying Sun;Jun-feng Guo;Da Yan Wang;Y. Shu
中科院分区:
其他
文献类型:
--
作者:
Qiang Sun;Na Lei;Jian Lu;R. Gao;Zi Li;Li Qi Liu;Ying Sun;Jun-feng Guo;Da Yan Wang;Y. Shu

文献摘要

相似文献

目的干扰素诱导的跨膜蛋白3(IFITM 3)是IFITM家族的重要成员。然而,其抗病毒作用的分子机制尚未完全阐明。最近对IFITM 3的研究,特别是那些关注先天性抗病毒防御机制的研究,表明IFITM 3影响人体的适应性免疫反应。本研究的目的是确定IFITM 3蛋白对体内流感感染的免疫控制的贡献。方法采用蛋白质组学、流式细胞术和免疫组织化学分析方法,并利用生物信息学工具,系统比较和分析Ifitm 3-/-和野生型小鼠肺内自然杀伤(NK)细胞数量、活化和免疫功能的差异。结果与野生型小鼠相比,Ifitm 3-/-小鼠发生更严重的炎症和凋亡反应。此外,在急性流感感染期间,Ifitm 3-/-小鼠肺中的NK细胞活化较高。结论基于我们的结果,我们推测在IFITM 3缺失的情况下NK细胞更容易被激活,增加了IFITM 3-/-小鼠的死亡率。
Objective Interferon-induced transmembrane protein 3 (IFITM3) is an important member of the IFITM family. However, the molecular mechanisms underlying its antiviral action have not been completely elucidated. Recent studies on IFITM3, particularly those focused on innate antiviral defense mechanisms, have shown that IFITM3 affects the body's adaptive immune response. The aim of this study was to determine the contribution of IFITM3 proteins to immune control of influenza infection in vivo. Methods We performed proteomics, flow cytometry, and immunohistochemistry analysis and used bioinformatics tools to systematically compare and analyze the differences in natural killer (NK) cell numbers, their activation, and their immune function in the lungs of Ifitm3-/- and wild-type mice. Results Ifitm3-/- mice developed more severe inflammation and apoptotic responses compared to wild-type mice. Moreover, the NK cell activation was higher in the lungs of Ifitm3-/- mice during acute influenza infection. Conclusions Based on our results, we speculate that the NK cells are more readily activated in the absence of IFITM3, increasing mortality in Ifitm3-/- mice.