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

Dev Comp Immunol. 2016 Dec:65:245-252. doi: 10.1016/j.dci.2016.07.012. Epub 2016 Jul 26.

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.

Keywords: Dendritic cell; Immunophenotype; PRRSV; Thl /Th2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptive Immunity*
  • Animals
  • Antigen Presentation
  • Arterivirus / physiology*
  • Arterivirus Infections / immunology*
  • Cell Differentiation
  • Cells, Cultured
  • Cytokines / genetics
  • Cytokines / metabolism
  • Dendritic Cells / immunology*
  • Dendritic Cells / virology
  • Histocompatibility Antigens / metabolism
  • Immune Evasion
  • Monocytes / immunology*
  • Swine
  • Th1-Th2 Balance
  • Transcriptome
  • Viral Load

Substances

  • Cytokines
  • Histocompatibility Antigens