In:
Science Immunology, American Association for the Advancement of Science (AAAS), Vol. 5, No. 50 ( 2020-08-14)
Kurzfassung:
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.
Materialart:
Online-Ressource
ISSN:
2470-9468
DOI:
10.1126/sciimmunol.aba4163
Sprache:
Englisch
Verlag:
American Association for the Advancement of Science (AAAS)
Publikationsdatum:
2020
