The frequencies of pDCs, which are major producers of IFN-β and IFN-α in vivo (47), increased in the periphery of αβR−/− mice but not αβR−/− λR−/− mice upon YFV-17D infection, suggesting a potential defect in the antiviral response of pDCs in αβR−/− λR−/− mice. Here, IFNA1 is linked to infection.