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https://repository.monashhealth.org/monashhealthjspui/handle/1/28966| Title: | Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease. | Authors: | Huber T.B.;Franzenburg S.;Koch-Nolte F.;Turner J.-E.;Riedel J.-H.;Huber S.;Gagliani N.;Wiech T.;Rohde H.;Bono M.R.;Bonn S.;Panzer U.;Mittrucker H.-W.;Krebs C.F.;Reimers D.;Zhao Y.;Paust H.-J.;Bartsch P.;Nunez 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. | Institution: | (Krebs, Paust, Bartsch, Hellmig, Kilian, Borchers, Enk, Zinke, Riedel, Panzer) III. Department of Medicine, Division of Translational Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (Krebs, Koch-Nolte, Turner, Huber, Gagliani, Huber, Bonn, Panzer, Mittrucker) Hamburg Center for Translational Immunology (HCTI), Hamburg, Germany (Reimers, Schmid, Klinge, Schmidt, Bertram, Koch-Nolte, Mittrucker) University Medical Center Hamburg-Eppendorf, Institute for Immunology, Hamburg, Germany (Zhao, Bonn) University Medical Center Hamburg-Eppendorf, Institute of Medical Systems Biology, Hamburg, Germany (Nunez) Fundacion Ciencia Vida, SantiagoChile (Rosemblatt, Wiech) Faculty of Medicine and Science, Universidad San Sebastian, Santiago, Chile (Becker, Wong, Puelles, Hoxha, Lindenmeyer, Cohen, Turner, Huber) III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (Puelles) Department of Nephrology, And Center for Inflammatory Diseases, Monash University, Monash Health, Melbourne, VIC, Australia (Stumpf, Kurts) Institutes of Molecular Medicine and Experimental Immunology (IMMEI), Rheinische Friedrich-Wilhelms-Universitat, Bonn, Germany (Meyer-Schwesinger) University Medical Center Hamburg-Eppendorf, Institute for Cellular and Integrative Physiology, Hamburg, Germany (Cohen) Nephrological Center, Medical Clinic and Policlinic IV, University of Munich, Munich, Germany (Rink) Department of Urology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (Franzenburg) Institute of Clinical Molecular Biology, Kiel University, Kiel, Germany (Huber, Gagliani) I.Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (Gagliani) Department of Medicine, Immunology and Allergy Unit, Karolinska Institute and University Hospital, Solna ,Stockholm 17176, Sweden (Panzer) University Medical Center Hamburg-Eppendorf, Institute for Pathology, Germany (Rohde) University Medical Center Hamburg-Eppendorf, Institute for Medical Microbiology, Virology and Hygiene, Hamburg, Germany (Bono) Department of Biology, Faculty of Sciences, Universidad de Chile, Santiago, Chile (Bonn) German Center for Neurodegenerative Diseases, Tubingen, Germany (Bonn) Center for Biomedical Ai, Hamburg, Germany | Issue Date: | 24-Nov-2020 | Copyright year: | 2020 | Publisher: | American Association for the Advancement of Science | Place of publication: | United States | Publication information: | Science Immunology. 5 (50) (no pagination), 2020. Article Number: 4163. Date of Publication: August 2020. | Journal: | Science Immunology | 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.Copyright © 2020 American Association for the Advancement of Science. All rights reserved. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1126/SCIIMMUNOL.ABA4163 | PubMed URL: | 32769171 [http://www.ncbi.nlm.nih.gov/pubmed/?term=32769171] | ISSN: | 2470-9468 (electronic) | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/28966 | Type: | Article | Subjects: | uropathogenic Escherichia coli animal experiment animal model animal tissue article *autoimmune disease Candida albicans CD4+ T lymphocyte controlled study cytokine production cytokine response disease exacerbation *glomerulonephritis human human cell human tissue immune response kidney biopsy Listeria monocytogenes listeriosis mouse nonhuman priority journal Staphylococcus aureus Staphylococcus aureus infection/dt [Drug Therapy] *Th17 cell ampicillin/dt [Drug Therapy] ampicillin/po [Oral Drug Administration] interleukin 17/ec [Endogenous Compound] *ANCA associated glomerulonephritis *tissue resident memory Th17 cell disease exacerbation *glomerulonephritis human human cell human tissue immune response kidney biopsy Listeria monocytogenes listeriosis mouse animal model priority journal Staphylococcus aureus Staphylococcus aureus infection / drug therapy *Th17 cell uropathogenic Escherichia coli animal experiment nonhuman animal tissue Article *autoimmune disease Candida albicans CD4+ T lymphocyte controlled study cytokine production cytokine response |
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