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Bertram, Tabea; Reimers, Daniel; Lory, Niels C; Schmidt, Constantin; Schmid, Joanna; C Heinig, Lisa; Bradtke, Peter; Rattay, Guido; Zielinski, Stephanie; Hellmig, Malte; Bartsch, Patricia; Rohde, Holger; Nuñez, Sarah; Rosemblatt, Mariana V; Bono, Maria Rosa; Gagliani, Nicola; Sandrock, Inga; Panzer, Ulf; Krebs, Christian F; Meyer-Schwesinger, Catherine; Prinz, Immo; Mittrücker, Hans-Willi
Proceedings of the National Academy of Sciences, 01/2023, Volume: 120, Issue: 1Journal Article
γδ T cells are involved in the control of infection, but their importance in protection compared to other T cells is unclear. We used a mouse model of systemic infection associated with high bacterial load and persistence in the kidney. Infection caused fulminant accumulation of γδ T cells in the kidney. Renal γδ T cells acquired tissue residency and were maintained in high numbers during chronic infection. At day 7, up to 50% of renal γδ T cells produced IL-17A in situ and a large fraction of renal γδ T cells remained IL-17A during chronic infection. Controlled depletion revealed that γδ T cells restricted renal replication in the acute infection and provided protection during chronic renal infection and upon reinfection. Our results demonstrate that kidney-resident γδ T cells are nonredundant in limiting local growth during chronic infection and provide enhanced protection against reinfection.
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