Partial Activation of Natural Killer and γδ T Cells by Classical Swine Fever Viruses Is Associated with Type I Interferon Elicited from Plasmacytoid Dendritic Cells
Published in
Clinical and Vaccine Immunology (formerly CDLI), July 2014
Vaccination with live attenuated classical swine fever virus (CSFV) vaccines can rapidly confer protection in the absence of neutralising antibodies. With a view to providing information on cellular mechanisms that may mediate this protection, we explored the interaction of porcine natural killer (NK) cells and γδ-T cells with CSFV. Both NK and γδ-T cells were refractory to infection with attenuated or virulent CSFV and no stimulatory effects, as assessed by expression of MHC class II (MHC-II), perforin and IFN-γ, were observed when cells were cultured in the presence of CSFV. Co-culture with CSFV and myeloid (mDCs) or plasmacytoid (pDCs) dendritic cells showed that the latter led to a partial activation of both NK and γδ-T cells, with up-regulation of MHC-II being observed. Analysis of cytokine expression by infected DC subsets suggested that this effect was due to IFN-α secreted by infected pDCs. These results were supported by ex-vivo analyses of NK and γδ-T cells in the tonsils and retro-pharyngeal lymph nodes from pigs that had been vaccinated with live attenuated CSFV and/or challenged with virulent CSFV. At 5 days post-challenge there was evidence of significant up-regulation of MHC-II but not perforin on NK and γδ-T cells, which was only observed following challenge of unvaccinated pigs and correlated with increased CSFV replication and IFN-α expression in both tonsils and serum. Together, these data suggest that it is unlikely that NK or γδ-T cells contribute to the cellular effector mechanisms induced by live attenuated CSFV.
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