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

Author

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

Published
2022
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3. Kidney-resident innate-like memory γδ T cells control chronic Staphylococcus aureus infection of mice.

Author

Bertram, Tabea, Reimers, Daniel, Lory, Niels C., Schmidt, Constantin, Schmid, Joanna, Heinig, Lisa C., 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., and Meyer-Schwesinger, Catherine

Subjects
STAPHYLOCOCCUS aureus infections, T cells
Abstract

γδ T cells are involved in the control of Staphylococcus aureus infection, but their importance in protection compared to other T cells is unclear. We used a mouse model of systemic S. aureus 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 S. aureus 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 S. aureus growth during chronic infection and provide enhanced protection against reinfection. [ABSTRACT FROM AUTHOR]

Published
2023
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4. Ecto-5′-Nucleotidase (CD73) Regulates the Survival of CD8+ T Cells

Author

Rosemblatt, Mariana V., primary, Parra-Tello, Brian, additional, Briceño, Pedro, additional, Rivas-Yáñez, Elizabeth, additional, Tucer, Suat, additional, Saavedra-Almarza, Juan, additional, Hörmann, Pilar, additional, Martínez, Brandon A., additional, Lladser, Álvaro, additional, Rosemblatt, Mario, additional, Cekic, Caglar, additional, Bono, María Rosa, additional, and Sauma, Daniela, additional

Published
2021
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5. CD73 Ectonucleotidase Restrains CD8+ T Cell Metabolic Fitness and Anti-tumoral Activity

Author

Briceño, Pedro, primary, Rivas-Yañez, Elizabeth, additional, Rosemblatt, Mariana V., additional, Parra-Tello, Brian, additional, Farías, Paula, additional, Vargas, Leonardo, additional, Simon, Valeska, additional, Cárdenas, César, additional, Lladser, Alvaro, additional, Salazar-Onfray, Flavio, additional, Elorza, Alvaro A., additional, Rosemblatt, Mario, additional, Bono, María Rosa, additional, and Sauma, Daniela, additional

Published
2021
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6. Pathogen-induced tissue-resident memory T H 17 (T RM 17) cells amplify autoimmune kidney disease

Author

Krebs, Christian F., primary, Reimers, Daniel, additional, Zhao, Yu, additional, Paust, Hans-Joachim, additional, Bartsch, Patricia, additional, Nuñez, Sarah, additional, Rosemblatt, Mariana V., additional, Hellmig, Malte, additional, Kilian, Christoph, additional, Borchers, Alina, additional, Enk, Leon U. B., additional, Zinke, Michael, additional, Becker, Martina, additional, Schmid, Joanna, additional, Klinge, Stefanie, additional, Wong, Milagros N., additional, Puelles, Victor G., additional, Schmidt, Constantin, additional, Bertram, Tabea, additional, Stumpf, Natascha, additional, Hoxha, Elion, additional, Meyer-Schwesinger, Catherine, additional, Lindenmeyer, Maja T., additional, Cohen, Clemens D., additional, Rink, Michael, additional, Kurts, Christian, additional, Franzenburg, Sören, additional, Koch-Nolte, Friedrich, additional, Turner, Jan-Eric, additional, Riedel, Jan-Hendrik, additional, Huber, Samuel, additional, Gagliani, Nicola, additional, Huber, Tobias B., additional, Wiech, Thorsten, additional, Rohde, Holger, additional, Bono, Maria Rosa, additional, Bonn, Stefan, additional, Panzer, Ulf, additional, and Mittrücker, Hans-Willi, additional

Published
2020
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7. P2X7 Receptor at the Crossroads of T Cell Fate

Author

Rivas-Yáñez, Elizabeth, primary, Barrera-Avalos, Carlos, additional, Parra-Tello, Brian, additional, Briceño, Pedro, additional, Rosemblatt, Mariana V., additional, Saavedra-Almarza, Juan, additional, Rosemblatt, Mario, additional, Acuña-Castillo, Claudio, additional, Bono, María Rosa, additional, and Sauma, Daniela, additional

Published
2020
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8. Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease.

Author

Krebs, Christian F., Reimers, Daniel, Zhao, Yu, Paust, Hans-Joachim, Bartsch, Patricia, Nuñez, Sarah, Rosemblatt, Mariana V., Hellmig, Malte, Kilian, Christoph, Borchers, Alina, Enk, Leon U. B., Zinke, Michael, Becker, Martina, Schmid, Joanna, Klinge, Stefanie, Wong, Milagros N., Puelles, Victor G., Schmidt, Constantin, Bertram, Tabea, and Stumpf, Natascha

Abstract

Autoimmunity promoter: Tissue-resident memory T (TRM) cells are involved in peripheral immunity against reinfection, but their role in autoimmunity is unclear. Krebs et al. examine the contribution of TRM cells in patients with antineutrophil cytoplasmic antibody (ANCA)–dependent glomerulonephritis (GN). They identified multiple T cell subsets in healthy kidney tissue biopsies, but a marked increase in CD4+ TRM cells was seen in kidney biopsies from patients with ANCA-GN. They infected mice with Staphylococcus aureus, which induced renal TH17 cells that had a TRM cell phenotype and persisted in kidney tissue. In a mouse model of crescentic GN, S. aureus infection aggravated kidney pathology and appeared to drive localized renal autoimmune responses. These findings provide critical insight into the role of CD4+ TRM cells in contributing to autoimmune disease. Although it is well established that microbial infections predispose to autoimmune diseases, the underlying mechanisms remain poorly understood. After infection, tissue-resident memory T (TRM) cells persist in peripheral organs and provide immune protection against reinfection. However, whether TRM cells participate in responses unrelated to the primary infection, such as autoimmune inflammation, is unknown. By using high-dimensional single-cell analysis, we identified CD4+ TRM cells with a TH17 signature (termed TRM17 cells) in kidneys of patients with ANCA-associated glomerulonephritis. Experimental models demonstrated that renal TRM17 cells were induced by pathogens infecting the kidney, such as Staphylococcus aureus, Candida albicans, and uropathogenic Escherichia coli, and persisted after the clearance of infections. Upon induction of experimental glomerulonephritis, these kidney TRM17 cells rapidly responded to local proinflammatory cytokines by producing IL-17A and thereby exacerbate renal pathology. Thus, our data show that pathogen-induced TRM17 cells have a previously unrecognized function in aggravating autoimmune disease. [ABSTRACT FROM AUTHOR]

Published
2020
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9. In Vitro-Generated Tc17 Cells Present a Memory Phenotype and Serve As a Reservoir of Tc1 Cells In Vivo

Author

Flores-Santibáñez, Felipe, primary, Cuadra, Bárbara, additional, Fernández, Dominique, additional, Rosemblatt, Mariana V., additional, Núñez, Sarah, additional, Cruz, Pablo, additional, Gálvez-Cancino, Felipe, additional, Cárdenas, J. César, additional, Lladser, Alvaro, additional, Rosemblatt, Mario, additional, Bono, María Rosa, additional, and Sauma, Daniela, additional

Published
2018
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