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@ARTICLE{Krebs:153351,
      author       = {Krebs, Christian F. and Reimers, Daniel and Zhao, Yu and
                      Paust, Hans-Joachim and Bartsch, Patricia and Nuñez, Sarah
                      and Rosemblatt, Mariana V. and Hellmig, Malte and Kilian,
                      Christoph and Borchers, Alina and Enk, Leon U. B. and Zinke,
                      Michael and Becker, Martina and Schmid, Joanna and Klinge,
                      Stefanie and Wong, Milagros N. and Puelles, Victor G. and
                      Schmidt, Constantin and Bertram, Tabea and Stumpf, Natascha
                      and Hoxha, Elion and Meyer-Schwesinger, Catherine and
                      Lindenmeyer, Maja T. and Cohen, Clemens D. and Rink, Michael
                      and Kurts, Christian and Franzenburg, Sören and Koch-Nolte,
                      Friedrich and Turner, Jan-Eric and Riedel, Jan-Hendrik and
                      Huber, Samuel and Gagliani, Nicola and Huber, Tobias B. and
                      Wiech, Thorsten and Rohde, Holger and Bono, Maria Rosa and
                      Bonn, Stefan and Panzer, Ulf and Mittrücker, Hans-Willi},
      title        = {{P}athogen-induced tissue-resident memory {T} {H} 17 ({T}
                      {RM} 17) cells amplify autoimmune kidney disease},
      journal      = {Science immunology},
      volume       = {5},
      number       = {50},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DZNE-2020-01348},
      pages        = {eaba4163},
      year         = {2020},
      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.},
      keywords     = {Animals / Antibodies, Antineutrophil Cytoplasmic:
                      immunology / Autoimmune Diseases: immunology / Autoimmune
                      Diseases: microbiology / Bacterial Infections: immunology /
                      CD4-Positive T-Lymphocytes: immunology / Candida albicans /
                      Candidiasis: immunology / Glomerulonephritis: immunology /
                      Glomerulonephritis: microbiology / Humans / Immunologic
                      Memory / Kidney: immunology / Male / Mice, Inbred DBA /
                      Mice, Transgenic / T-Lymphocyte Subsets: immunology},
      cin          = {AG Bonn 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1410003},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32769171},
      doi          = {10.1126/sciimmunol.aba4163},
      url          = {https://pub.dzne.de/record/153351},
}