Until recently, innate and acquired immunity were perceived to be rather independent of each other. It was obvious by 1992 that alveolar macrophages and natural killer (NK) cells, by releasing tumour necrosis factor-α and interferon-γ (IFN-γ), respectively, play a central role in the innate response, whereas T-helper (h)1 and Th2 T-cells downregulate each other by their respective cytokines, IFN-γ and interleukin-4 (IL-4), during acquired immunity. It is now becoming clear that the divergence into Th1 and Th2 cells is regulated by the innate immune response, mainly through the release of IL-12 by macrophages and the release of IL-4 by CD4+ NK1.1 cells. As dendritic cells initiate specific T-cell acquired immunity, understanding the influence of cytokines produced by the innate immune system on dendritic cell maturation and function will be an important goal of future research. As macrophages are the main source of cytokine production in the lung during bacterial infection, the important role of bacterial lipopolysaccharides and superantigens in both innate and acquired immunity will be discussed.