Previous studies have shown that Batf3−/− mice, which lack CD8α+ cDCs, are unable to control infection following challenge with strains of T. gondii that have intermediate virulence due to defective recognition of the parasite at early time points after infection, resulting in reduced IL-12 production and hence defective NK cell activation (11, 36) However, in Batf3−/− mice, CD8 T cell priming can still occur through presentation of soluble antigens (38), as well as direct presentation, suggesting that adaptive immunity may only be partially affected. This evidence concerns the gene BATF3 and infection.