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¹ German Rheumatism Research Center Berlin, 10117 Berlin, Germany
² Department of Rheumatology and Clinical Immunology, ³ Institute of Pathology, Charité-University Medicine Berlin, 10117 Berlin, Germany
⁴ Department of Pathology/RCIS, ⁵ Medical Clinic I (Gastroenterology, Rheumatology, Infectiology), Charité-University Medicine Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany
⁶ Institute of Immunology, Friedrich Schiller University Jena, Medical School, 07740 Jena, Germany
⁷ Cecilie Vogt Clinic for Neurology in the HKBB, Charité–University Medicine Berlin, and Max Delbrück Center for Molecular Medicine, 10117 Berlin, Germany
⁸ Department of Medicine, Division of Hepatology and Gastroenterology, Charité-University Medicine Berlin, Humboldt University of Berlin, 13344 Berlin, Germany
⁹ Department of Virology and Developmental Genetics, Ben Gurion University of the Negev, Beer Sheva 84105, Israel
¹⁰ Max Planck Institute for Molecular Genetics, Department of Vertebrate Genomics, 14195 Berlin, Germany

CORRESPONDENCE Andreas Radbruch: radbruch{at}drfz.de

The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor B (NF-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-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-, IL-2, and tumor necrosis factor-, and ameliorated Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis.

U. Niesner and I. Albrecht contributed equally to this paper.

© 2008 Niesner et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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