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白细胞介素 16 缺乏增强了针对甲型流感病毒感染的 Th1 和细胞毒性 T 淋巴细胞反应。

IL16 deficiency enhances Th1 and cytotoxic T lymphocyte response against influenza A virus infection.

机构信息

Department of Clinical Laboratory, Children's Hospital of Fudan University, Shanghai, China.

Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

出版信息

Biosci Trends. 2020 Jan 20;13(6):516-522. doi: 10.5582/bst.2019.01286. Epub 2019 Dec 18.

DOI:10.5582/bst.2019.01286
PMID:31852865
Abstract

Influenza A virus (IAV) is the major cause of seasonal epidemics and flu outbreaks worldwide. Given that interleukin 16 (IL16) can regulate T cell function and is one of the signature markers for virus infection including IAV infection, the impact of IL16 on IAV-induced T cell immune response hasn't been elucidated yet. In this paper, we infected wild type and IL16 knockout (KO) mice with IAV and analyzed the immunity of mice by flow cytometry. We observed an increase in the percentage of T helper (Th) 1 cells in the spleens of IL16 KO mice and elevation of IFN-γ and TNF-ɑ secretion from CD8 T cells in the lungs and spleens of IL16 KO mice in response to IAV infection. Moreover, the expression of major histocompatibility complex II which represents the maturation of dendritic cells (DCs) was upregulated in the lungs of IL16 KO mice. Taken together, our study suggests that IL16 deficiency enhanced Th1 and cytotoxic T lymphocyte response as well as DC maturation upon IAV infection, which provides new insight into the host regulation of T cell immune responses during IAV infection.

摘要

甲型流感病毒(IAV)是全球季节性流行和流感爆发的主要原因。鉴于白细胞介素 16(IL16)可以调节 T 细胞功能,是包括 IAV 感染在内的病毒感染的特征标志物之一,IL16 对 IAV 诱导的 T 细胞免疫反应的影响尚未阐明。在本文中,我们用 IAV 感染野生型和 IL16 敲除(KO)小鼠,并通过流式细胞术分析了小鼠的免疫反应。我们观察到,在 IAV 感染后,IL16 KO 小鼠的脾脏中 Th1 细胞的比例增加,并且 IL16 KO 小鼠的肺和脾中的 CD8 T 细胞分泌 IFN-γ和 TNF-ɑ增加。此外,代表树突状细胞(DC)成熟的主要组织相容性复合体 II 的表达在 IL16 KO 小鼠的肺部上调。综上所述,我们的研究表明,在 IAV 感染时,IL16 缺失增强了 Th1 和细胞毒性 T 淋巴细胞反应以及 DC 成熟,这为宿主在 IAV 感染期间对 T 细胞免疫反应的调节提供了新的见解。

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