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Subset‐dependent modulation of dendritic cell activity by circovirus type 2
Author(s) -
Vincent Isabelle E.,
Carrasco Carlos P.,
GuzylackPiriou Laurence,
Herrmann Brigitte,
McNeilly Francis,
Allan Gordon M.,
Summerfield Artur,
McCullough Kenneth C.
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2005.02165.x
Subject(s) - biology , microbiology and biotechnology , porcine circovirus , interferon , dendritic cell , myeloid , immune system , context (archaeology) , immunology , virology , virus , paleontology
Summary Viral interactions with dendritic cells (DCs) have important consequences for immune defence function. Certain single‐stranded DNA viruses that associate with a number of species, including humans and pigs, exhibit interesting characteristics in this context. Porcine circovirus type 2 (PCV2) can persist within myeloid DCs in the absence of virus replication. Internalization was observed with both conventional blood DCs and plasmacytoid DCs [natural interferon‐producing cells (NIPCs)], as well as DC precursors. This PCV2–DC interaction neither induced nor inhibited DC differentiation. The maturation of myeloid DCs induced by a cocktail of interferon‐α/tumour necrosis factor‐α (IFN‐α/TNF‐α), and the ability to process and present antigen to T lymphocytes, remained intact in the presence of PCV2. The virus was clearly internalized by the DCs, a process noted with both mature and immature cells. This suggested a non‐macropinocytic uptake, confirmed by an insensitivity to wortmannin but sensitivity to cytochalasin D, chlorpromazine and bafilomycin. Nevertheless, PCV2 was immunomodulatory, being effected through the reaction of NIPC to danger signals. When NIPCs responded to the CpG‐oligonucleotide (CpG‐ODN), their costimulatory function which induces myeloid DC maturation was clearly impaired by the presence of PCV2. This was caused by a PCV2‐induced inhibition of the IFN‐α and TNF‐α normally produced following interaction with CpG‐ODN. Thus, the immunomodulatory activity of PCV2 is mediated through the disruption of NIPC function. This would impair the maturation of associated myeloid DC and have major implications for the efficient recognition of viral and bacterial danger signals, favouring the establishment of infections additional to that of PCV2.