The role of porcine reproductive and respiratory syndrome virus infection in immune phenotype and Th1/Th2 balance of dendritic cells. (December 2016)

• Record Type: Journal Article
• Authors: Liu, Jinling; Wei, Shu; Liu, Lixia; Shan, Fengping; Zhao, Yujun; Shen, Guoshun
• Is Part Of: Developmental and comparative immunology. Volume 65(2016)
• Page Start: 245
• Page End: 252
• Publication Date: 2016-12
• Subjects: PRRSV -- Dendritic cell -- Immunophenotype -- Thl /Th2; Immunology -- Periodicals; Developmental immunology -- Periodicals; 616.079
• DOI: 10.1016/j.dci.2016.07.012
• Languages: English
• ISSNs: 0145-305X

Abstract

Abstract: 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. Highlights: PRRSV LN strain infection could impair the normal antigen presentation ability of Mo-DCs of porcine peripheral blood. PRRSV LN strain infection could influence the mature of Mo-DCs by down-regulating the expressions of costimulatory molecules. PRRSV LN could lead to inadequate in the adaptive immune response in early PRRSV infection by causing the Thl/Th2 unbalance.