Murine + ˇT cells participate in innate immune response against infection of the intracellular bacterium Listeria monocytogenes. In the present report, we analyzed the mechanism of the + ˇT cell-mediated response against L. monocytogenes infection. + ˇT cell-enriched spleen cells of L. monocytogenes-infected mice produced IFN-+ in vitro in response to L. monocytogenes-infected spleen cells. The IFN-+ production was abrogated by depletion of V + 1 + + ˇT cells. IFN-+ production of the V + 1 + + ˇT cells in response to L. monocytogenesinfected spleen cells required IL-12. However, addition of Fab fragment of anti-TCR + monoclonal antibodies (mAb) failed to block the response, suggesting that the response requires no TCR-mediated antigen recognition. Interestingly, V + 1 + + ˇT cells of naive mice also produced IFN-+ in response to L. monocytogenes-infected spleen cells in an IL-12dependent manner. Furthermore, the IL-12 receptor (IL-12R) gene was expressed on the V + 1 + + ˇT cells of naive mice as well as those of L. monocytogenes-infected mice although naive § g T cells lack IL-12R expression. All the results suggest that the V + 1 + + ˇT cells participate in immune surveillance against intracellular bacterial infection through quick production of IFN-+ in response to infection-induced IL-12 without antigen-driven clonal expansion and maturation.