Although it is generally assumed that T-cell receptor (TCR) γ/δ cells participate in protection against intracellular microbial pathogens, their impact remains controversial. In our study, young (14-day-old) mice lacking TCRγ/δ cells were far more susceptible to Listeria monocytogenes than wild-type (WT) mice of the same age. The number of interferon gamma (IFN-γ) producers responsible for antilisterial resistance was significantly higher among natural killer (NK)1+ TCRγ/δ cells than among NK1 TCRγ/δ cells. Endogenous IFN-γ neutralization increased susceptibility of young WT mice to L. monocytogenes infection. Liver was a major residence of peripheral NK1+ TCRγ/δ cells, whereas NK1 TCR γ/δ cells were broadly distributed in various lymphoid organs. Numbers of both NK1+ and NK1 TCRγ/δ cells increased in the liver of WT mice prior to TCRα/β cells and represented a substantial population in early life (14 days after birth). Virtually all NK1+ TCRγ/δ cells expressed activation markers, whereas substantial numbers of NK1 TCRγ/δ cells showed a naive phenotype. We conclude that TCRγ/δ cells play a critical role in protection against L. monocytogenes in the early life of mice, probably because their TCRα/β cell compartment is not fully competent. For this antibacterial function, we assign NK1+ TCRγ/δ cells a more important role than their NK1 cognates.