Although both DCs and other myeloid cells showed higher levels of infection after anti-IFNAR1 mAb treatment, experiments with knockout and conditional knockout mice showed that (i) CD11c+ DCs were principally responsible for the enhanced RRV-specific CD8+ T-cell response; (ii) DC cross-presentation did not explain this enhanced response; (iii) DCs appeared to be directly infected; and (iv) loss of type I IFN signaling in DC1s was sufficient to augment the polyfunctionality of the RRV-specific CD8+ T-cell response. The gene discussed is IFNAR1; the disease is infection.