Kidney-resident innate-like memory γδ T cells control chronic Staphylococcus aureus infection of mice

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 ki...

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Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 120; no. 1; p. e2210490120
Main Authors: 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
Format: Journal Article
Language:English
Published: United States National Academy of Sciences 03-01-2023
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Summary: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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1T.B. and D.R. contributed equally to this work.
Edited by Tak Mak, University of Toronto, Toronto, Canada; received June 18, 2022; accepted October 20, 2022
ISSN:0027-8424
1091-6490
1091-6490
DOI:10.1073/pnas.2210490120