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Tanja Diana Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Hans-Peter Holthoff AdvanceCor GmbH, Martinsried, Germany

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Julia Fassbender AdvanceCor GmbH, Martinsried, Germany

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Christian Wüster Endocrine Laboratory and Practice Prof. Wüster, Mainz, Germany

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Michael Kanitz Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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George J. Kahaly Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Martin Ungerer AdvanceCor GmbH, Martinsried, Germany

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]. The autoimmune process that occurs in GD involves both T cells and B cells, which results in the production of autoantibodies to the TSH receptor (TSHR-Ab). The clinical phenotype of GD is induced by unregulated stimulation of thyroid cells and TSHR

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George J. Kahaly Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Luigi Bartalena Department of Medicine and Surgery, University of Insubria, Varese, Italy

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Lazlo Hegedüs Department of Endocrinology and Metabolism, Odense University Hospital, Odense, Denmark

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Laurence Leenhardt Thyroid and Endocrine Tumors Unit, Pitié Salpêtrière Hospital, Sorbonne University, Paris, France

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Kris Poppe Endocrine Unit, CHU Saint-Pierre, Université Libre de Bruxelles (ULB), Brussels, Belgium

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Simon H. Pearce Department of Endocrinology, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom

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–60 years, with an increased incidence among African Americans [ 8 ]. GD is an organ-specific autoimmune disease whose major manifestations are owing to circulating autoantibodies (Ab) that stimulate the thyroid-stimulating hormone receptor (TSH-R) leading

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Sita Virakul Departments of Immunology, University Medical Center Rotterdam
Internal Medicine, Erasmus MC, University Medical Center Rotterdam

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Leendert van Steensel Departments of Immunology, University Medical Center Rotterdam

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Virgil A.S.H. Dalm Departments of Immunology, University Medical Center Rotterdam

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Dion Paridaens Rotterdam Eye Hospital, Rotterdam, The Netherlands
Department of Ophthalmology, Geneva University Hospitals, Geneva, Switzerland

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P. Martin van Hagen Departments of Immunology, University Medical Center Rotterdam
Internal Medicine, Erasmus MC, University Medical Center Rotterdam
Rotterdam Eye Hospital, Rotterdam, The Netherlands

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Willem A. Dik Departments of Immunology, University Medical Center Rotterdam

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hyaluronan production by orbital fibroblasts, suggesting that TSHR stimulating autoantibodies contribute to development and severity of GO through orbital fibroblast activating properties [ 2 ]. Of the three PDGF-isoforms involved in GO it was found that PDGF-AB

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Tanja Diana Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Paul D. Olivo Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri, USA

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Yie-Hwa Chang Mediomics, LLC, St. Louis, Missouri, USA

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Christian Wüster Endocrine Laboratory and Practice Prof. Wüster, Mainz, Germany

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Michael Kanitz Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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George J. Kahaly Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Introduction Autoantibodies against the thyrotropin receptor (TSH-R-Ab) play an important role in the pathogenesis of autoimmune thyroid diseases [ 1 - 5 ]. These functional antibodies demonstrate different effects on the TSH-R and can either

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George J. Kahaly Johannes Gutenberg University Medical Center, Mainz, Germany

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Autoantibodies (Ab) to the TSH receptor (TSHR) are responsible for many of the clinical manifestations of Graves' disease (GD) and are specific biomarkers of this autoimmune thyroid disorder (AITD) [ 1 , 2 , 3 ]. These Ab can be measured

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C. Daumerie Departments of Endocrinology, Université catholique de Louvain, University Hospital St-Luc, Brussels, Belgium

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A. Boschi Departments of Ophthalmology, Université catholique de Louvain, University Hospital St-Luc, Brussels, Belgium

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P. Perros Department of Endocrinology, Royal Victoria Infirmary, Newcastle upon Tyne, UK

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, and the demonstration of a relationship between the level of antibodies to the TSHR (TSHR-Ab) and the development of GO indicates that autoimmune reactions against the TSHR may be a prime cause of GO. TSHR-Ab are present in the serum of the majority of

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Tanja Diana Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Christian Wüster Endocrine Laboratory Prof. Wüster, Mainz, Germany

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Paul D. Olivo Department of Microbiology, Washington University, St. Louis, Missouri, USA

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Angelica Unterrainer Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Jochem König Endocrine Laboratory Prof. Wüster, Mainz, Germany

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Michael Kanitz Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Artur Bossowski Department of Pediatrics, Endocrinology, and Diabetology, Medical University of Byalistok, Bialystok, Poland

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Brigitte Decallonne Division of Clinical and Experimental Endocrinology, UZ Leuven, Leuven, Belgium

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George J. Kahaly Molecular Thyroid Research Laboratory, Department of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany

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Introduction Antibodies (Ab) to the thyroid-stimulating hormone receptor (TSHR) may mimic [ 1 - 3 ] or block [ 4 ] the action of TSH or be functionally neutral [ 5 ]. TSHR stimulating Ab (TSAb) are responsible for many of the clinical

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Gerd Krause Structural Biology, Leibniz-Forschungsinstitut für molekulare Pharmakologie (FMP), Berlin, Germany

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Anja Eckstein Department of Ophthalmology, University Hospital Essen, Essen, Germany

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Ralf Schülein Protein Trafficking, Leibniz-Forschungsinstitut für molekulare Pharmakologie (FMP), Berlin, Germany

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Introduction TSH-Receptor, Graves’ Disease and Graves’ Orbitopathy The thyrotropin receptor or thyroid-stimulating hormone (TSH) receptor (TSHR) is mainly expressed in follicular epithelial cells of the thyroid gland [ 1 ]. TSHR activation

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Sébastien Verdickt Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Falco Van Nes Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Carolien Moyson Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Toon Maes Department of Endocrinology, Imeldaziekenhuis Bonheiden, Bonheiden, Belgium

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Paul Van Crombrugge Department of Endocrinology, OLV Ziekenhuis Aalst-Asse-Ninove, Aalst, Belgium

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Annick Van den Bruel Department of Endocrinology, AZ Sint Jan Brugge, Brugge, Belgium

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Brigitte Decallonne Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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-stimulating hormone receptor antibody (TSH-R Ab) titer or radiation absorbed dose ( 2 , 3 , 4 , 5 , 6 , 7 , 8 ). Thyroid peroxidase antibodies (TPO Abs) are associated with autoimmune thyroid disease, and their measurement is helpful in the diagnostic workup

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Anke Schlüter Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, Essen, Germany
Department of Oto-Rhino-Laryngology – Head and Neck Surgery, University Hospital Essen, Essen, Germany

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Anja K. Eckstein Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, Essen, Germany
Department of Ophthalmology, University Hospital Essen, Essen, Germany

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Alexandra Brenzel Imaging Center Essen (IMCES), Institute for Experimental Immunology and Imaging, University Hospital Essen, Essen, Germany

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Mareike Horstmann Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, Essen, Germany

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Stephan Lang Department of Oto-Rhino-Laryngology – Head and Neck Surgery, University Hospital Essen, Essen, Germany

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Utta Berchner-Pfannschmidt Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, Essen, Germany

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J. Paul Banga Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, Essen, Germany

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Salvador Diaz-Cano Department of Histopathology, King’s College Hospital NHS, London, United Kingdom

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Introduction Graves disease (GD) is caused by autoantibodies that induce hyperthyroidism by mimicking the action of TSH and activating the TSH receptor (TSHR). The defining component of hyperthyroidism is thyroid follicular hyperplasia

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