TY  - JOUR
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
TI  - Pathogen-induced tissue-resident memory T H 17 (T RM 17) cells amplify autoimmune kidney disease
JO  - Science immunology
VL  - 5
IS  - 50
SN  - 2470-9468
CY  - Washington, DC
PB  - AAAS
M1  - DZNE-2020-01348
SP  - eaba4163
PY  - 2020
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.
KW  - Animals
KW  - Antibodies, Antineutrophil Cytoplasmic: immunology
KW  - Autoimmune Diseases: immunology
KW  - Autoimmune Diseases: microbiology
KW  - Bacterial Infections: immunology
KW  - CD4-Positive T-Lymphocytes: immunology
KW  - Candida albicans
KW  - Candidiasis: immunology
KW  - Glomerulonephritis: immunology
KW  - Glomerulonephritis: microbiology
KW  - Humans
KW  - Immunologic Memory
KW  - Kidney: immunology
KW  - Male
KW  - Mice, Inbred DBA
KW  - Mice, Transgenic
KW  - T-Lymphocyte Subsets: immunology
LB  - PUB:(DE-HGF)16
C6  - pmid:32769171
DO  - DOI:10.1126/sciimmunol.aba4163
UR  - https://pub.dzne.de/record/153351
ER  -