Characterization of the CD8 T cell response to Salmonella typhimurium infection in mice

Abstract

Salmonella typhimurium (ST) causes gasteroenteritis in humans and typhoid-like disease in mice. Since CD8 T cells facilitate acquired immunity, we evaluated the development and function of the CD8 T cell response against ST. Responses were compared to the acute intracellular pathogen, Listeria monocytogenes (LM). Because ST replicates within phagosomes and causes chronic infection, it was hypothesized that CD8 T cell priming may be muted and dysfunctional. While LM-induced CD8 T cells differentiated rapidly and displayed a mainly central-memory phenotyope in the long-term, CD8 T cells failed to become activated rapidly during ST infection and differentiated mainly into an effector/effector-memory phenotype. While the CD8 T cells induced against ST were functional, owing to the delay in CD8 T cell activation during ST infection, even conventional memory CD8 T cells failed to respond rapidly. Thus, the phagosomal lifestyle may allow escape from CD8+ T cells, conferring a survival advantage to the pathogen.