Partial activation of natural killer and gammadelta T cells by classical swine fever viruses is associated with type I interferon elicited from plasmacytoid dendritic cells
Vaccination with live attenuated classical swine fever virus (CSFV) vaccines can rapidly confer protection in the absence of neutralizing antibodies. With an aim of providing information on the cellular mechanisms that may mediate this protection, we explored the interaction of porcine natural killer (NK) cells and gammadelta T cells with CSFV. Both NK and gammadelta T cells were refractory to infection with attenuated or virulent CSFV, and no stimulatory effects, as assessed by the expression of major histocompatibility complex (MHC) class II (MHC-II), perforin, and gamma interferon (IFN-gamma), were observed when the cells were cultured in the presence of CSFV. Coculture with CSFV and myeloid dendritic cells (mDCs) or plasmacytoid dendritic cells (pDCs) showed that pDCs led to a partial activation of both NK and gammadelta T cells, with upregulation of MHC-II being observed. An analysis of cytokine expression by infected DC subsets suggested that this effect was due to IFN-alpha secreted by infected pDCs. These results were supported by ex vivo analyses of NK and gammadelta T cells in the tonsils and retropharyngeal lymph nodes from pigs that had been vaccinated with live attenuated CSFV and/or virulent CSFV. At 5 days postchallenge, there was evidence of significant upregulation of MHC-II but not perforin on NK and gammadelta T cells, which was observed only following a challenge of the unvaccinated pigs and correlated with increased CSFV replication and IFN-alpha expression in both the tonsils and serum. Together, these data suggest that it is unlikely that NK or gammadelta T cells contribute to the cellular effector mechanisms induced by live attenuated CSFV.