In the case of cultured hepatocytes, Salmonella growth is inhibited by the CpG DNA treatment, whereas in the case of human monocyte-derived macrophages it has no effect. In hepatocytes, an enhanced ROS production after the CpG DNA treatment has been attributed to be the cause of decreased Salmonella burden. However, in bone marrow derived macrophages CpG-antagonist act in a TLR-9 independent manner to inhibit Salmonella killing. Our study is the first report which indicates that in the dendritic cells CpG DNA enhances Salmonella killing. We went ahead to check the exact mechanism behind, and noticed that CpG induction leads to an enhanced generation of ROS from the infected cells. To look into the mechanism behind this phenomenon, we blocked the ROS production in the ligand treated infected dendritic cells. Under that condition this enhanced killing was no more observed. This finding clearly demonstrates that the CpG treatment allows better killing of Salmonella in a ROS dependent manner. Several report have documented that Salmonella inhibits antigen presentation from DC to MHC class II molecules. This effect was dependent on the induction of inducible NO synthase by DC and on the function of virulence genes in SPI2, as SPI2 deficient bacterial infection led to an enhanced amount of both CD4 and CD8 cells. SPI-2 encoded proteins like SifA, SspH2, SlrP, PipB2, and SopD2 were found to be important for the interference with antigen presentation, whereas SseF and SseG contributed to a lesser extent to this phenotype. Published data clearly outline the pivotal role of ROS in the antigen presenting cells. Maintaining the redox potential is extremely important for macrophages and DCs to present antigen in the context of MHC molecules. Oxidative stress has been reported to modulate the signal transduction pathways in lymphocytes. It has been further observed that antioxidants like NAC, quercetin and polyphenolic compounds directly inhibit B cell mediated antigen presentation by inhibiting NFkb activation. Moreover, the antigen specific DC-T cell interaction can be specifically blocked by modulating the redox potential of DCs. These findings led us to look into the antigen presentation capacity of the CpG treated infected cells as the cells were producing higher amount of ROS. So, we went ahead to measure the antigen presentation by the help of a mixed lymphocytic reaction. The role of CpG DNA has been well documented as an adjuvant in multiple experimental and clinical vaccines. Therefore, our study indicates that CpG DNA can be used as an adjuvant to design new vaccines with increased efficiency AMN107 against Salmonella. Our next aim was to check the role of CpG in aiding cross presentation in the Salmonella infected DC.