A Critical Role of T–Cell Receptor γ/δ Cells in Antibacterial Protection in Mice Early in Life

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Abstract
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.

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