During Listeria monocytogenes infection, Irf4−/− CD8+ T cells retained a “precursor-like” state with impaired acquisition of an effector phenotype that was similar to that of Prdm1−/− CD8+ T cells, suggesting that IRF-4 functions upstream of Blimp-1 in the development of protective effector CD8+ T cells during an immune response against an intracellular bacterium [69]. This evidence concerns the gene IRF4 and listeriosis.