δ T cells are important for the early control of West Nile virus (WNV) dissemination. Here, we investigated the role of δ T cells in the regulation of CD4+ T-cell response following a WNV challenge. Splenic dendritic cells (DCs) of WNV-infected δ T-cell-deficient (TCRδ−/−) mice displayed lower levels of CD40, CD80, CD86 and major histocompatibility complex (MHC) class II expression and interleukin-12 (IL-12) production than those of wild-type mice. Naïve DCs cocultured with WNV-infected δ T cells showed enhanced levels of costimulatory molecules, MHC class II expression and IL-12 production. Further, coculture of CD4+ T cells from OT II transgenic mice with DCs of ... More
δ T cells are important for the early control of West Nile virus (WNV) dissemination. Here, we investigated the role of δ T cells in the regulation of CD4+ T-cell response following a WNV challenge. Splenic dendritic cells (DCs) of WNV-infected δ T-cell-deficient (TCRδ−/−) mice displayed lower levels of CD40, CD80, CD86 and major histocompatibility complex (MHC) class II expression and interleukin-12 (IL-12) production than those of wild-type mice. Naïve DCs cocultured with WNV-infected δ T cells showed enhanced levels of costimulatory molecules, MHC class II expression and IL-12 production. Further, coculture of CD4+ T cells from OT II transgenic mice with DCs of WNV-infected TCRδ−/− mice induced less interferon- (IFN-) and IL-2 production than with those of wild-type controls. Viral antigens were detected in WNV-infected δ T cells.WNV infection or toll-like receptor (TLR) agonist treatment of δ T cells induced the production of IFN-, tumor necrosis factor- and IL-6, which are known to promote DC maturation. Nevertheless, the levels of TLRs 2, 3, 4 and 7 expression of WNV-infected δ T cells were not different from those of noninfected cells. Overall, these data suggest that WNV-induced δ T-cell activation promotes DC maturation and initiates CD4+ T-cell priming.
