Suppression of dendritic cell and T-cell activation by the pRST⁹⁸ Salmonella plasmid.

Salmonella evades host immune response via the expression of a variety of pathogenic factors. The 'pRST98' plasmid of Salmonella enterica serotype Typhi (S. Typhi) is involved in conferring the multidrug‑resistance and virulence of S. typhi. However, its specific effect on host‑cell function has remained elusive. Dendritic cells (DCs) are key regulators of immune responses. The present study therefore aimed to investigate whether pRST98 may target DCs involved in mediating the adaptive immune response. In vivo experiments with Salmonella enterica serotype Typhimurium χ3337 and χ3337/pRST98 revealed that pRST98 may influence multiple important functions of murine DCs, including maturation, survival and cytokine production. In addition, pRST98 markedly contributed to decreasing T‑cell activation. These data suggested that by targeting the aforementioned functions of DCs, pRST98 may partially overturn the adaptive immune defense mechanisms of the host, which are required for elimination of this pathogen from infected tissues. This may contribute to the evasion of host adaptive immune responses by S. Typhi and therefore provide a target for the prevention and treatment of typhoid fever.