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

• Published in: Immunology Vol. 102; no. 1; pp. 94 - 102
• Main Authors: Ikebe, H., Yamada, H., Nomoto, M., Takimoto, H., Nakamura, T., Sonoda, K.‐H., Nomoto, K.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.01.2001; Blackwell Science Inc
• Subjects: Original
• ISSN: 0019-2805; 1365-2567
• DOI: 10.1046/j.1365-2567.2001.01149.x

Summary After intraperitoneal inoculation with Listeria monocytogenes, γδ T 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/Vδ1+TCR and plays a regulatory role in resolution of inflammation.