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

  • Tabea Bertram
  • , Daniel Reimers
  • , Niels C. Lory
  • , Constantin Schmidt
  • , Joanna Schmid
  • , Lisa C. Heinig
  • , Peter Bradtke
  • , Guido Rattay
  • , Stephanie Zielinski
  • , Malte Hellmig
  • , Patricia Bartsch
  • , Holger Rohde
  • , Sarah Nuñez
  • , Mariana V. Rosemblatt
  • , Maria Rosa Bono
  • , Nicola Gagliani
  • , Inga Sandrock
  • , Ulf Panzer
  • , Christian F. Krebs
  • , Catherine Meyer-Schwesinger
  • Immo Prinz, Hans-Willi Mittrücker

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

13 Citas (Scopus)

Resumen

<jats:p> γδ T cells are involved in the control of <jats:italic>Staphylococcus aureus</jats:italic> infection, but their importance in protection compared to other T cells is unclear. We used a mouse model of systemic <jats:italic>S. aureus</jats:italic> 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 <jats:sup>+</jats:sup> during chronic infection. Controlled depletion revealed that γδ T cells restricted renal <jats:italic>S. aureus</jats:italic> 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 <jats:italic>S. aureus</jats:italic> growth during chronic infection and provide enhanced protection against reinfection. </jats:p>

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