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.