The role of innate response of CD8 memory T cell during infections is now well established. However, while the mechanisms that govern its induction and mode of actions in particular IFNg secretion are more and more elucidated, little is known about the regulation of this response.To address this issue, we have established mice models of Salmonella typhimurium (ST) infection, in which we were able to follow the fate of unrelated memory CD8 T cells. These models allowed us to show the consistent and reproducible death of the memory CD8 T cells upon infection. Using different strains of KO mice we could show the dependence of this process on Bcl-2 expression and could exclude type IFN as mediator of this process. The death of non-cognate memory CD8 T cells during the ST infection was associated with a decrease in the level of IFNg measured both in spleen and in the serum of infected mice. The mechanism of this process, its potential role in the regulation of the CD8 innate response and its physiological relevance during the infection is currently under investigation, and will be assessed in other infections.