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          Institute: MPI für molekulare Genetik     Collection: Department of Vertebrate Genomics     Display Documents



  history
ID: 411201.0, MPI für molekulare Genetik / Department of Vertebrate Genomics
Autoregulation of Th1-mediated inflammation by twist1
Authors:Niesner, Uwe; Albrecht, Inka; Janke, Marko; Doebis, Cornelia; Loddenkemper, Christoph; Lexberg, Maria H.; Eulenburg, Katharina; Kreher, Stephan; Koeck, Juliana; Baumgrass, Ria; Bonhagen, Kerstin; Kamradt, Thomas; Enghard, Philipp; Humrich, Jens Y.; Rutz, Sascha; Schulze-Topphoff, Ulf; Aktas, Orhan; Bartfeld, Sina; Radbruch, Helena; Hegazy, Ahmed N.; Löhning, Max; Baumgart, Daniel C.; Duchmann, Rainer; Rudwaleit, Martin; Häupl, Thomas; Gitelman, Inna; Krenn, Veit; Gruen, Joachim; Sieper, Jochen; Zeitz, Martin; Wiedenmann, Bertram; Zipp, Frauke; Hamann, Alf; Janitz, Michal; Scheffold, Alexander; Burmester, Gerd R.; Chang, Hyun D.; Radbruch, Andreas
Language:English
Date of Publication (YYYY-MM-DD):2008-08
Title of Journal:Journal of Experimental Medicine
Journal Abbrev.:J Exp Med
Volume:205
Issue / Number:8
Start Page:1889
End Page:1901
Copyright:© 2008 Niesner et al
Review Status:not specified
Audience:Experts Only
Abstract / Description:The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor {kappa}B (NF-{kappa}B)–dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We show that twist1 is expressed by activated T helper (Th) 1 effector memory (EM) cells. Induction of twist1 in Th cells depended on NF-{kappa}B, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 was transient after T cell receptor engagement, and increased upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression was characteristic of repeatedly restimulated EM Th cells, and thus of the pathogenic memory Th cells characteristic of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn's disease or ulcerative colitis expressed high levels of twist1. Expression of twist1 in Th1 lymphocytes limited the expression of the cytokines interferon-{gamma}, IL-2, and tumor necrosis factor-{alpha}, and ameliorated Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis.
Comment of the Author/Creator:e-Mail: radbruch@drfz.de
External Publication Status:published
Document Type:Article
Communicated by:Hans Lehrach
Affiliations:MPI für molekulare Genetik
External Affiliations:German Rheumatism Research Center Berlin, 10117 Berlin, Germany
Department of Rheumatology and Clinical Immunology
Institute of Pathology, Charité-University Medicine Berlin, 10117 Berlin, Germany
Department of Pathology/RCIS, 5 Medical Clinic I (Gastroenterology, Rheumatology, Infectiology), Charité-University Medicine Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany
Institute of Immunology, Friedrich Schiller University Jena, Medical School, 07740 Jena, Germany
Cecilie Vogt Clinic for Neurology in the HKBB, Charité–University Medicine Berlin, and Max Delbrück Center for Molecular Medicine, 10117 Berlin, Germany
Department of Medicine, Division of Hepatology and Gastroenterology, Charité-University Medicine Berlin, Humboldt University of Berlin, 13344 Berlin, Germany
Department of Virology and Developmental Genetics, Ben Gurion University of the Negev, Beer Sheva 84105, Israel
Identifiers:ISSN:0022-1007
DOI:10.1084/jem.20072468
URL:http://jem.rupress.org/cgi/reprint/205/8/1889
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