Journal Article

DZNE-2020-01348

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Pathogen-induced tissue-resident memory T H 17 (T RM 17) cells amplify autoimmune kidney disease

Krebs, C. F. (Corresponding author) ; 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. ; Stumpf, N. ; Hoxha, E. ; Meyer-Schwesinger, C. ; Lindenmeyer, M. T. ; Cohen, C. D. ; Rink, M. ; Kurts, C. ; Franzenburg, S. ; Koch-Nolte, F. ; Turner, J.-E. ; Riedel, J.-H. ; Huber, S. ; Gagliani, N. ; Huber, T. B. ; Wiech, T. ; Rohde, H. ; Bono, M. R. ; Bonn, S.DZNE* ; Panzer, U. ; Mittrücker, H.-W. (Corresponding author)

2020
AAAS Washington, DC

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Please use a persistent id in citations: doi:10.1126/sciimmunol.aba4163

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.

Keyword(s): Animals (MeSH) ; Antibodies, Antineutrophil Cytoplasmic: immunology (MeSH) ; Autoimmune Diseases: immunology (MeSH) ; Autoimmune Diseases: microbiology (MeSH) ; Bacterial Infections: immunology (MeSH) ; CD4-Positive T-Lymphocytes: immunology (MeSH) ; Candida albicans (MeSH) ; Candidiasis: immunology (MeSH) ; Glomerulonephritis: immunology (MeSH) ; Glomerulonephritis: microbiology (MeSH) ; Humans (MeSH) ; Immunologic Memory (MeSH) ; Kidney: immunology (MeSH) ; Male (MeSH) ; Mice, Inbred DBA (MeSH) ; Mice, Transgenic (MeSH) ; T-Lymphocyte Subsets: immunology (MeSH)

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Contributing Institute(s):

1. Computational analysis of biological networks (AG Bonn 1)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2020

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Database coverage:
; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Essential Science Indicators ; IF >= 30 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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