The role of porcine reproductive and respiratory syndrome virus infection in immune phenotype and Th1/Th2 balance of dendritic cells

被引:16
作者
Liu, Jinling [1 ]
Wei, Shu [2 ]
Liu, Lixia [1 ]
Shan, Fengping [3 ]
Zhao, Yujun [1 ]
Shen, Guoshun [1 ]
机构
[1] Shenyang Agr Univ, Coll Anim Sci & Vet Med, Key Lab Zoonosis Liaoning Prov, Shenyang 110866, Peoples R China
[2] Prevent Ctr Anim Dis LiaoNing Prov, 95 Renhe Rd, Shenyang 110164, Peoples R China
[3] China Med Univ, Basic Sch Med, Dept Immunol, 92 North Second Rd, Shenyang 110001, Peoples R China
关键词
PRRSV; Dendritic cell; Immunophenotype; Th1/Th2; MATURATION; RESPONSES; PIGS; ACTIVATION; EXPRESSION; BMDCS; PRRSV;
D O I
10.1016/j.dci.2016.07.012
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
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-gamma and TNF-alpha 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-gamma and TNF-alpha secretion results in Th1/Th2 imbalance. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:245 / 252
页数:8
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