The protective role of T-cell receptor Vγ1+ T cells in primary infection with Listeria monocytogenes

We have previously reported that the T-cell receptor (TCR) γδ+ T cells increase in mice infected with an intracellular bacteria Listeria monocytogenes, and the cells predominantly express Vδ6 and Vγ1 genes. In this study, we used a monoclonal antibody (mAb) specific to TCR Vγ1 to estimate the frequency of Vγ1+ T cells and we discuss their significance in protection against L. monocytogenes. The spleen, liver and peritoneal exudate cells from mice intraperitoneally infected with L. monocytogenes were analysed by flow cytometry. In all the organs investigated, Vγ1+ cells increased predominantly among TCR γδ+ T cells at an early phase (day 5–7) of the infection. To elucidate the significance of the Vγ1+ T cells in the protection against L. monocytogenes, mice were depleted of TCR Vγ1+γδ T cells or all TCR γδ+ T cells by intraperitoneal inoculation of anti-Vγ1 mAb or anti-pan TCR γδ mAb, respectively, before infection with L. monocytogenes. The bacterial growth in the spleen and the liver examined on day 5 after the infection increased significantly by the depletion of TCR Vγ1+ T cells. The numbers of L. monocytogenes in TCR Vγ1+ T-cell-depleted mice were nearly the same as in mice depleted of all TCR γδ+ T cells. These results demonstrated that Vγ1+ T cells are the predominant population of γδ T cells in protection against L. monocytogenes at the early phase of the primary infection

Interleukin-15 production at the early stage after oral infection with Listeria monocytogenes in mice

We previously reported that exogenous interleukin-15 (IL-15) induces proliferation and activation of intestinal intraepithelial lymphocytes (i-IEL) in naive mice. To investigate the ability of endogenous IL-15 to stimulate i-IEL in vivo, we monitored i-IEL and intestinal epithelial cells (i-EC) in mice after an oral infection with Listeria monocytogenes. Although the populations of αβ and γδ i-IEL were not significantly changed after the oral infection, the expression level of interferon-γ (IFN-γ) was increased both at transcriptional and protein levels, and a conversely marked decrease in interleukin-4 (IL-4) was detected in the i-IEL on day 1 after infection as compared with before infection. The T helper 1 (Th1)-biased response of i-IEL coincided with a peak response of IL-15 production in the i-EC after oral infection. These results suggested that IL-15 produced from i-EC may be at least partly involved in the stimulation of i-IEL to produce IFN-γ after oral infection with L. monocytogenes