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Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease

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Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease. / 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; Stumpf, Natascha; Hoxha, Elion; Meyer-Schwesinger, Catherine; Lindenmeyer, Maja T; Cohen, Clemens D; Rink, Michael; Kurts, Christian; Franzenburg, Sören; Koch-Nolte, Friedrich; Turner, Jan-Eric; Riedel, Jan-Hendrik; Huber, Samuel; Gagliani, Nicola; Huber, Tobias B; Wiech, Thorsten; Rohde, Holger; Bono, Maria Rosa; Bonn, Stefan; Panzer, Ulf; Mittrücker, Hans-Willi.

In: SCI IMMUNOL, Vol. 5, No. 50, eaba4163, 07.08.2020.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Krebs, CF, Reimers, D, Zhao, Y, Paust, H-J, Bartsch, P, Nuñez, S, Rosemblatt, MV, Hellmig, M, Kilian, C, Borchers, A, Enk, LUB, Zinke, M, Becker, M, Schmid, J, Klinge, S, Wong, MN, Puelles, VG, Schmidt, C, Bertram, T, Stumpf, N, Hoxha, E, Meyer-Schwesinger, C, Lindenmeyer, MT, Cohen, CD, Rink, M, Kurts, C, Franzenburg, S, Koch-Nolte, F, Turner, J-E, Riedel, J-H, Huber, S, Gagliani, N, Huber, TB, Wiech, T, Rohde, H, Bono, MR, Bonn, S, Panzer, U & Mittrücker, H-W 2020, 'Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease', SCI IMMUNOL, vol. 5, no. 50, eaba4163. https://doi.org/10.1126/sciimmunol.aba4163

APA

Krebs, C. F., Reimers, D., Zhao, Y., Paust, H-J., Bartsch, P., Nuñez, S., Rosemblatt, M. V., Hellmig, M., Kilian, C., Borchers, A., Enk, L. U. B., Zinke, M., Becker, M., Schmid, J., Klinge, S., Wong, M. N., Puelles, V. G., Schmidt, C., Bertram, T., ... Mittrücker, H-W. (2020). Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease. SCI IMMUNOL, 5(50), [eaba4163]. https://doi.org/10.1126/sciimmunol.aba4163

Vancouver

Krebs CF, Reimers D, Zhao Y, Paust H-J, Bartsch P, Nuñez S et al. Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease. SCI IMMUNOL. 2020 Aug 7;5(50). eaba4163. https://doi.org/10.1126/sciimmunol.aba4163

Bibtex

@article{bbdaa261a77c4b70982c16f5b2dee081,
title = "Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease",
abstract = "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.",
author = "Krebs, {Christian F} and Daniel Reimers and Yu Zhao and Hans-Joachim Paust and Patricia Bartsch and Sarah Nu{\~n}ez and Rosemblatt, {Mariana V} and Malte Hellmig and Christoph Kilian and Alina Borchers and Enk, {Leon U B} and Michael Zinke and Martina Becker and Joanna Schmid and Stefanie Klinge and Wong, {Milagros N} and Puelles, {Victor G} and Constantin Schmidt and Tabea Bertram and Natascha Stumpf and Elion Hoxha and Catherine Meyer-Schwesinger and Lindenmeyer, {Maja T} and Cohen, {Clemens D} and Michael Rink and Christian Kurts and S{\"o}ren Franzenburg and Friedrich Koch-Nolte and Jan-Eric Turner and Jan-Hendrik Riedel and Samuel Huber and Nicola Gagliani and Huber, {Tobias B} and Thorsten Wiech and Holger Rohde and Bono, {Maria Rosa} and Stefan Bonn and Ulf Panzer and Hans-Willi Mittr{\"u}cker",
note = "Copyright {\textcopyright} 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.",
year = "2020",
month = aug,
day = "7",
doi = "10.1126/sciimmunol.aba4163",
language = "English",
volume = "5",
journal = "SCI IMMUNOL",
issn = "2470-9468",
publisher = "American Association for the Advancement of Science",
number = "50",

}

RIS

TY - JOUR

T1 - Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease

AU - Krebs, Christian F

AU - Reimers, Daniel

AU - Zhao, Yu

AU - Paust, Hans-Joachim

AU - Bartsch, Patricia

AU - Nuñez, Sarah

AU - Rosemblatt, Mariana V

AU - Hellmig, Malte

AU - Kilian, Christoph

AU - Borchers, Alina

AU - Enk, Leon U B

AU - Zinke, Michael

AU - Becker, Martina

AU - Schmid, Joanna

AU - Klinge, Stefanie

AU - Wong, Milagros N

AU - Puelles, Victor G

AU - Schmidt, Constantin

AU - Bertram, Tabea

AU - Stumpf, Natascha

AU - Hoxha, Elion

AU - Meyer-Schwesinger, Catherine

AU - Lindenmeyer, Maja T

AU - Cohen, Clemens D

AU - Rink, Michael

AU - Kurts, Christian

AU - Franzenburg, Sören

AU - Koch-Nolte, Friedrich

AU - Turner, Jan-Eric

AU - Riedel, Jan-Hendrik

AU - Huber, Samuel

AU - Gagliani, Nicola

AU - Huber, Tobias B

AU - Wiech, Thorsten

AU - Rohde, Holger

AU - Bono, Maria Rosa

AU - Bonn, Stefan

AU - Panzer, Ulf

AU - Mittrücker, Hans-Willi

N1 - Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

PY - 2020/8/7

Y1 - 2020/8/7

N2 - 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.

AB - 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.

U2 - 10.1126/sciimmunol.aba4163

DO - 10.1126/sciimmunol.aba4163

M3 - SCORING: Journal article

C2 - 32769171

VL - 5

JO - SCI IMMUNOL

JF - SCI IMMUNOL

SN - 2470-9468

IS - 50

M1 - eaba4163

ER -