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淋巴毒素受体对于 IFN 诱导的鸟苷酸结合蛋白的上调和感染后生存是必需的。

The Lymphotoxin Receptor Is Essential for Upregulation of IFN-Induced Guanylate-Binding Proteins and Survival after Infection.

机构信息

Institute of Medical Microbiology and Hospital Hygiene, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany.

Molecular Medicine II, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany.

出版信息

Mediators Inflamm. 2017;2017:7375818. doi: 10.1155/2017/7375818. Epub 2017 Aug 6.

DOI:10.1155/2017/7375818
PMID:28845089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5563413/
Abstract

Lymphotoxin receptor (LTR) signaling plays an important role in efficient initiation of host responses to a variety of pathogens, encompassing viruses, bacteria, and protozoans via induction of the type I interferon response. The present study reveals that after infection, LTR mice show a substantially reduced survival rate when compared to wild-type mice. LTR mice exhibit an increased parasite load and a more pronounced organ pathology. Also, a delayed increase of serum IL-12p40 and a failure of the protective IFN response in LTR mice were observed. Serum NO levels in LTR animals rose later and were markedly decreased compared to wild-type animals. At the transcriptional level, LTR animals exhibited a deregulated expression profile of several cytokines known to play a role in activation of innate immunity in infection. Importantly, expression of the IFN-regulated murine guanylate-binding protein (mGBP) genes was virtually absent in the lungs of LTR mice. This demonstrates clearly that the LTR is essential for the induction of a type II IFN-mediated immune response against . The pronounced inability to effectively upregulate host defense effector molecules such as GBPs explains the high mortality rates of LTR animals after infection.

摘要

淋巴毒素受体 (LTR) 信号在宿主对各种病原体（包括病毒、细菌和原生动物）的有效起始反应中发挥重要作用，通过诱导 I 型干扰素反应来实现。本研究表明，感染后，与野生型小鼠相比，LTR 小鼠的存活率显著降低。LTR 小鼠表现出寄生虫载量增加和更明显的器官病理学。此外，还观察到 LTR 小鼠血清 IL-12p40 的增加延迟和保护性 IFN 反应的失败。LTR 动物的血清 NO 水平升高较晚，且明显低于野生型动物。在转录水平上，LTR 动物表现出几种细胞因子的表达谱失调，这些细胞因子已知在 感染中激活固有免疫中发挥作用。重要的是，LTR 小鼠肺中 IFN 调节的鼠鸟苷酸结合蛋白 (mGBP) 基因的表达几乎不存在。这清楚地表明，LTR 对于诱导针对 的 II 型 IFN 介导的免疫反应是必不可少的。宿主防御效应分子（如 GBPs）的上调能力明显受损，解释了 LTR 动物在 感染后的高死亡率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/560b/5563413/8d0c10c47767/MI2017-7375818.009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/560b/5563413/914f7cbd121a/MI2017-7375818.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/560b/5563413/471b4e0eefd7/MI2017-7375818.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/560b/5563413/8d0c10c47767/MI2017-7375818.009.jpg

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