TGEV nonstructural protein ORF3b upregulates the expression of SLA-DR at the transcriptional level in monocyte-derived porcine dendritic cells.

IF 2.6 4区 医学 Q3 IMMUNOLOGY
Hang Liu, Mengyao Ma, Xinhao Jia, Mengwei Qian, Bo Pang, Muzi Li, Honglei Zhang, Shijie Ma, Lanlan Zheng
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引用次数: 0

Abstract

Transmissible gastroenteritis virus (TGEV) is a porcine intestinal pathogenic coronavirus that can cause acute intestinal diseases in pigs, especially in suckling piglets under two weeks of age, with a mortality rate of 100%. Dendritic cells (DCs) are important antigen-presenting cells (APCs) that are essential for the initiation and modulation of immune responses in animals. In this study, we used monocyte-derived porcine DCs as an in vitro model of APCs to further study the pathogenic mechanism of TGEV. Our results demonstrated that TGEV successfully replicates in monocyte-derived porcine DCs, whereas UV-inactivated TGEV failed to infect these cells. Importantly, TGEV infection of DCs led to significant upregulation of swine leukocyte antigen II DR (SLA-DR), a key molecule in the major histocompatibility complex class II (MHC-II) family. We further demonstrated that the ORF3b nonstructural protein of TGEV significantly enhances SLA-DR expression at the transcriptional level in porcine DCs. This study provides new insights into the pathogenic mechanisms of TGEV.

TGEV非结构蛋白ORF3b可在转录水平上上调单核细胞衍生猪树突状细胞中SLA-DR的表达。
传染性胃肠炎病毒(TGEV)是一种猪肠道致病性冠状病毒,可引起猪的急性肠道疾病,尤其是两周龄以下的哺乳仔猪,死亡率高达 100%。树突状细胞(DC)是重要的抗原递呈细胞(APC),对动物免疫反应的启动和调节至关重要。在本研究中,我们使用单核细胞衍生的猪 DCs 作为体外 APCs 模型,进一步研究 TGEV 的致病机制。我们的研究结果表明,TGEV 能在单核细胞衍生的猪 DCs 中成功复制,而紫外线灭活的 TGEV 却不能感染这些细胞。重要的是,TGEV 感染 DCs 会导致猪白细胞抗原 II DR(SLA-DR)显著上调,而猪白细胞抗原 II DR 是主要组织相容性复合体 II 类(MHC-II)家族中的一个关键分子。我们进一步证实,TGEV 的 ORF3b 非结构蛋白在转录水平上显著增强了猪 DCs 中 SLA-DR 的表达。这项研究为了解 TGEV 的致病机制提供了新的视角。
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来源期刊
Microbes and Infection
Microbes and Infection 医学-病毒学
CiteScore
12.60
自引率
1.70%
发文量
90
审稿时长
40 days
期刊介绍: Microbes and Infection publishes 10 peer-reviewed issues per year in all fields of infection and immunity, covering the different levels of host-microbe interactions, and in particular: the molecular biology and cell biology of the crosstalk between hosts (human and model organisms) and microbes (viruses, bacteria, parasites and fungi), including molecular virulence and evasion mechanisms. the immune response to infection, including pathogenesis and host susceptibility. emerging human infectious diseases. systems immunology. molecular epidemiology/genetics of host pathogen interactions. microbiota and host "interactions". vaccine development, including novel strategies and adjuvants. Clinical studies, accounts of clinical trials and biomarker studies in infectious diseases are within the scope of the journal. Microbes and Infection publishes articles on human pathogens or pathogens of model systems. However, articles on other microbes can be published if they contribute to our understanding of basic mechanisms of host-pathogen interactions. Purely descriptive and preliminary studies are discouraged.
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