Journal
SCIENCE IMMUNOLOGY
Volume 5, Issue 50, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aba4163
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Funding
- DFG [SFB1192, SFB1286, SFBTR57]
- Deutsche Nierenstiftung
- Deutsche Gesellschaft fur Nephrologie
- Werner Otto Stiftung
- eMed Consortia Fibromap from the Federal Ministry of Education and Research
- Conicyt [AFB 170004, Conicyt/FONDEQUIP/EQM140016]
- Else Kroner-Fresenius Foundation
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Although it is well established that microbial infections predispose to autoimmune diseases, the underlying mechanisms remain poorly understood. After infection, tissue-resident memory T (T-RM) cells persist in peripheral organs and provide immune protection against reinfection. However, whether T-RM 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(+) T-RM cells with a T(H)17 signature (termed T(RM)17 cells) in kidneys of patients with ANCA-associated glomerulonephritis. Experimental models demonstrated that renal T(RM)17 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 T(RM)17 cells rapidly responded to local proinflammatory cytokines by producing IL-17A and thereby exacerbate renal pathology. Thus, our data show that pathogen-induced T(RM)17 cells have a previously unrecognized function in aggravating autoimmune disease.
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