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干扰素诱导跨膜蛋白 3 可预防小鼠急性流感发病。

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

机构信息

School of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen 510275, Guangdong, China;National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Prevention and Control, Beijing 102206, China.

National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Prevention and Control, Beijing 102206, China;Chaoyang District Center for Disease Prevention and Control, Beijing 100021, China.

出版信息

Biomed Environ Sci. 2020 May 20;33(5):295-305. doi: 10.3967/bes2020.041.

DOI:10.3967/bes2020.041
PMID:32553073
Abstract

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 .

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 -/- and wild-type mice.

RESULTS

-/- mice developed more severe inflammation and apoptotic responses compared to wild-type mice. Moreover, the NK cell activation was higher in the lungs of -/- 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 -/- mice.

摘要

目的

干扰素诱导跨膜蛋白 3(IFITM3)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 IFITM3 的研究,特别是针对先天抗病毒防御机制的研究表明,IFITM3 影响机体的适应性免疫反应。本研究旨在确定 IFITM3 蛋白对流感感染免疫控制的贡献。

方法

我们进行了蛋白质组学、流式细胞术和免疫组织化学分析,并使用生物信息学工具对 -/- 和野生型小鼠肺部自然杀伤(NK)细胞数量、其激活及其免疫功能的差异进行了系统比较和分析。

结果

与野生型小鼠相比,-/- 小鼠在流感感染急性期肺部炎症和细胞凋亡反应更严重。此外,在急性流感感染期间,-/- 小鼠肺部 NK 细胞的激活更高。

结论

基于我们的结果,我们推测在没有 IFITM3 的情况下,NK 细胞更容易被激活,从而增加 -/- 小鼠的死亡率。

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