Liu Jinling, Wei Shu, Liu Lixia, Shan Fengping, Zhao Yujun, Shen Guoshun
Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, PR China.
The Preventive Center of Animal Disease of LiaoNing Province, No.95, Renhe Road, Shenbei District, Shenyang 110164, PR China.
Dev Comp Immunol. 2016 Dec;65:245-252. doi: 10.1016/j.dci.2016.07.012. Epub 2016 Jul 26.
The aim of this study was to characterize the immune response of dendritic cells derived from monocytes (Mo-DCs) in the porcine peripheral blood following infection with porcine reproductive and respiratory syndrome virus (PRRSV). Viral load assays indicated that PRRSV efficiently infected Mo-DCs but failed to replicate, whereas PRRSV infection of Mo-DCs decreased the expression of SLA-I, SLA-II, CD80 and CD40 compared with those of mock Mo-DCs. Furthermore, we analyzed the cytokine profiles using quantitative RT-PCR and ELISA. Results indicated apparent changes in IL-10 and IL-12 p40 expression but not in IFN-γ and TNF-α among Mo-DCs infected with PRRSV and uninfected Mo-DCs. Additionally, flow cytometry analysis of the altered Mo-DCs together with IL-4 and GM-CSF induction for 7days revealed the typical morphology and phenotype with 91.73% purity before infection with PRRSV. Overall, our data demonstrate that PRRSV impaired the normal antigen presentation of Mo-DCs and led to inadequate adaptive immune response by down-regulating the expression of SLA-I,SLA-II, CD80 and CD40. Enhanced Th2 -type cytokine IL-10 secretion and reduced Th1-type cytokines IL-12p40,IFN-γ and TNF-α secretion results in Th1/Th2 imbalance.
本研究的目的是表征猪外周血中源自单核细胞的树突状细胞(Mo-DC)在感染猪繁殖与呼吸综合征病毒(PRRSV)后的免疫反应。病毒载量检测表明,PRRSV能有效感染Mo-DC,但无法复制,而与未感染PRRSV的对照Mo-DC相比,PRRSV感染的Mo-DC中SLA-I、SLA-II、CD80和CD40的表达降低。此外,我们使用定量逆转录聚合酶链反应和酶联免疫吸附测定分析了细胞因子谱。结果表明,在感染PRRSV的Mo-DC和未感染的Mo-DC中,IL-10和IL-12 p40的表达有明显变化,但IFN-γ和TNF-α没有变化。此外,对改变后的Mo-DC进行流式细胞术分析,并诱导IL-4和粒细胞-巨噬细胞集落刺激因子7天,结果显示在感染PRRSV之前,其具有典型的形态和表型,纯度为91.73%。总体而言,我们的数据表明,PRRSV损害了Mo-DC的正常抗原呈递,并通过下调SLA-I、SLA-II、CD80和CD40的表达导致适应性免疫反应不足。Th2型细胞因子IL-10分泌增加,Th1型细胞因子IL-12p40、IFN-γ和TNF-α分泌减少,导致Th1/Th2失衡。