AP-1 family transcription factor that controls the differentiation of CD8(+) thymic conventional dendritic cells in the immune system. Acts via the formation of a heterodimer with JUN family proteins that recognizes and binds DNA sequence 5'-TGA[CG]TCA-3' and regulates expression of target genes. Required for development of CD8-alpha(+) classical dendritic cells (cDCs) and related CD103(+) dendritic cells that cross-present antigens to CD8 T-cells and produce interleukin-12 (IL12) in response to pathogens. Heterodimer; heterodimerizes with JUN family proteins. Interacts with JUN. Highly expressed in CD8-alpha(+) classical dendritic cells (cDCs), with low to absent expression in other immune cells and non-immune tissues. Selective loss of CD8-alpha(+) classical dendritic cells (cDCs) and CD103(+) dendritic cells, without abnormalities in other hematopoietic cell types or architecture. Dendritic cells are defective in cross-presentation, and mice lack virus-specific CD8(+) T-cell responses to West Nile virus. Mice also show reduced priming of CD8 T-cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. Mice are extremely susceptible to T.gondii infection, with decreased production of interleukin-12 (IL12) and interferon-gamma. In contrast, mice are more resistant to L.monocytogenes infection. The increased protection toward L.monocytogenes infection in mice lacking Batf3 suggests that CD8-alpha(+) classical dendritic cells (cDCs) and CD103(+) dendritic cells are an entry point for infection by L.monocytogenes. Belongs to the bZIP family.