Batf3 is a transcription factor that impacts the development of CD103 tissue-resident dendritic cells (DCs). However, whether Batf3 is absolutely required for the development of CD8 DCs remains controversial. Id2 is required for CD8 DC development. Here we show that bone marrow chimeric mice with a deletion of Id2 in the CD11c compartment lose the ability to reject a skin graft expressing a non-self protein antigen or mount a delayed hypersensitivity response. In contrast, Batf3 mice remained competent for skin graft rejection and delayed hypersensitivity, and retained a CD8 DC population with markers characteristic of the CD11b DC lineage, including CD11b, CD4 and CD172α, as well as the key regulator transcription factor IRF4, but lacked IRF8 expression. CD8 DCs in Batf3 mice took up and cleaved protein antigen and larger particles but were unable to phagocytose dying cells, a characteristic feature to the CD8 DC lineage. These data clarify a requirement for CD8 lineage DCs to induce effectors of neo-antigen-driven skin graft rejection, and improve our understanding of DC subtype commitment by demonstrating that in the absence of Batf3 CD8 DCs can change their fate and become CD11b DCs.