These results are in good agreement with the reported profound defect of IRF8 mutant mice in the DCs compartment, as they lack both CD11c+CD8α+ DCs and pDCs, and the small number of CD11c+CD8α+ and CD8α− DCs present in these mice remain immature and fail to up-regulate co-stimulatory molecules and produce key cytokines in response to microbial products in vitro and in vivo during pulmonary tuberculosis [18], [26]. The gene discussed is CD8A; the disease is pulmonary tuberculosis.