Effect of porcine circovirus type 2 (PCV2) on the function of splenic CD11c+ dendritic cells in mice

Effect of porcine circovirus type 2 (PCV2) on the function of splenic CD11c+ dendritic cells in mice Porcine circovirus-associated disease (PCVAD) caused by porcine circovirus type 2 (PCV2) is an important disease in the global pig industry. Dendritic cells (DCs) are the primary immune cells capable of initiating adaptive immune responses as well as major target cells of PCV2. To determine whether PCV2 affects the immune functions of DCs, we evaluated the expression of endocytosis and co-stimulatory molecules on DCs (CD11c+) from PCV2-infected mouse spleen by flow cytometry (FCM). We also analyzed the main cytokines secreted by DCs (CD11c+) and activation of CD4+ and CD8+ T cells by DCs (CD11c+) through measurement of cytokine secretion, using ELISA. Compared with control mice, PCV2 did not affect the endocytic activity of DCs but it significantly enhanced TNF-α secretion and markedly decreased IFN-α secretion. Subsets of CD40+, MHCII+ CD40+ and CD137L+ CD86+ DCs did not increase obviously, but MHCII+ CD40- and CD137L- CD80+/CD86+ DCs increased significantly in PCV2-infected mouse spleen. Under the stimulation of DCs from PCV2-infected mouse, secretion of IFN-γ by CD4+ and CD8+ T cells and of IL-12 by CD8+ T cells was significantly lower than in control mice, while secretion of IL-4 by CD4+ T cells was remarkably higher. These results indicate that PCV2 modulates cytokine secretion and co-stimulatory molecule expression of DCs, and alters activation of CD4+ and CD8+ T cells by DCs. The immunomodulatory effects of PCV2 on DCs might be related to the host’s immune dysfunction and persistent infection with this virus. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Effect of porcine circovirus type 2 (PCV2) on the function of splenic CD11c+ dendritic cells in mice

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Publisher
Springer Vienna
Copyright
Copyright © 2017 by Springer-Verlag Wien
Subject
Biomedicine; Virology; Medical Microbiology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-017-3221-8
Publisher site
See Article on Publisher Site

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