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

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

*Autor correspondiente de este trabajo

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

67 Citas (Scopus)

Resumen

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.

Idioma originalInglés
Número de artículo4163
PublicaciónScience Immunology
Volumen5
N.º50
DOI
EstadoPublicada - 2020

Nota bibliográfica

Publisher Copyright:
© 2020 American Association for the Advancement of Science. All rights reserved.

Áreas temáticas de ASJC Scopus

  • Inmulogía y alergología
  • Inmunología

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