Persistent infection with Listeria monocytogenes in the kidney induces anti-inflammatory invariant fetal-type γδ T cells

Abstract

After intraperitoneal inoculation with Listeria monocytogenes, γδT cells appear in the peritoneal cavity preceding the appearance of αβ T cells. Such γδ T cells predominantly express T-cell receptor (TCR)Vγ1/Vδ6, develop through an extrathymic pathway, and contribute to host defence against the bacteria. We have observed a gradual increase in γδ T cells in kidneys of mice after intrarenal inoculation with L. monocytogenes, which resulted in an unusually long-lasting local infection. In this study, we examined the characteristics and the roles of the γδ T cells induced in this model. It was found that these γδ T cells predominantly expressed TCRVγ6/Vδ1 with canonical junctional sequences identical to those expressed on fetal thymocytes. Although depletion of such γδ T cells in vivo did not affect the number of bacteria, it resulted in histologically exacerbated inflammation in the kidneys. These results indicate that a persistent infection with L. monocytogenes in kidneys induces a different kind of γδ T cell from that induced after intraperitoneal infection. The former expresses invariant fetal-type Vγ6/VδI+TCR and plays a regulatory role in resolution of inflammation.