New advances in MS XL880 technologies afford even greater depth of coverage than reported in the earlier study. By combining knowledge of the proteome adaptation triggered by variation of principle environmental signals with existing transcriptome data, we obtained a more complete understanding of the changes occurring within B. burgdorferi as it responds to these environmental cues. This information provides us with important insight into potential candidate proteins which are changed as the organism prepares to infect the next host. Dendritic cells are specialized antigen presenting cells which constantly screen the environment for foreign particles and engulf them via a variety of ways like phagocytosis, macropinocytosis, caveolin-mediated or clathrin-dependent endocytosis. DCs function at the dividing line of innate and adaptive immunity and regulate the T cell response. DCs capture antigens in the peripheral tissues and present the processed antigen via the major histocompatibility complex I and II receptors. Salmonella in its turn is a very successful pathogen. It is a facultative intracellular pathogen and resides in macrophages and DCs by virtue of its pathogenicity island encoded virulence factors which are required for intracellular survival, replication and for the efficient colonization of deeper tissues. Salmonella is capable of causing symptoms ranging from self limiting diarrhea and localized gastrointestinal inflammation to the systemic typhoid fever. The mice model of infection mimics the pathogenesis of human typhoid fever. Toll like receptors are germ line receptors expressed on DCs and recognize infectious agents through the various moieties present on them and act as a bridge between innate and adaptive immunity. Their localization is determined by the nature of the ligand that they bind to. For instance, Toll like receptor-9 is localized in the late endosomes or lysosomes, where it detects unmethylated CpG motifs in double stranded DNA. Ligand receptor engagement leads to the docking of adaptor molecules like MyD88 to TLRs and recruitment of proteins belonging to the IRAK family. This ultimately leads to the NFkb activation and gene expression for the production of inflammatory cytokines like IL-6, IL-12 and TNF-a which lead to further recruitment of successive waves of immature DCs and monocytes to the portals of pathogen entry. Therefore, TLR activation helps in mounting a more prominent T cell response, better killing of the pathogen and thus utilizing TLR signaling could be an effective strategy to clear the invading pathogen. The same has been shown in cultured hepatocytes where CpG treatment led to an increased TLR-9 expression.