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Salmonella enterica serovar Typhi is associated with a disseminated febrile illness in humans, termed typhoid fever, whileSalmonella enterica serovar Typhimurium causes localized gastroenteritis in immunocompetent individuals. One of the genetic differences between both pathogens is the presence inS . Typhi of TviA, a regulatory protein that shuts down flagellin (FliC) expression when bacteria transit from the intestinal lumen into the intestinal mucosa. Here we investigated the consequences of TviA-mediated flagellum gene regulation on flagellin-specific CD4 T cell responses in a mouse model ofS . Typhimurium infection. Introduction of theS . TyphitviA gene intoS . Typhimurium suppressed antigen presentation of dendritic cells to flagellin-specific CD4 T cellsin vitro . Furthermore, TviA-mediated repression of flagellin expression impaired the activation and proliferation of naive flagellin-specific CD4 T cells in Peyer's patches and mesenteric lymph nodes, which was accompanied by increased bacterial dissemination to the spleen. We conclude that TviA-mediated repression of flagellin expression reduces antigen availability, thereby weakening flagellin-specific CD4 T cell responses.

Salmonella enterica Serovar Typhi Impairs CD4 T Cell Responses by Reducing Antigen Availability