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Susanne Neumann Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Bethesda, Bethesda, Maryland, USA

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Christine C. Krieger Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Bethesda, Bethesda, Maryland, USA

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Marvin C. Gershengorn Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Bethesda, Bethesda, Maryland, USA

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-Igs) was inhibited by some, but not all, IGF-1R-blocking antibodies (see below) [ 4 , 5 , 7 , 11 ]; and (4) TSHR and IGF-1R were shown to be in close proximity to each other scaffolded by β-arrestin 1, which was required for TSHR/IGF-1R crosstalk [ 12

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000511538
Volume/Issue:
Volume 9: Issue 1_Suppl
Free access
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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and thyroid-related antibodies. Bioassay for Blocking TSHR Antibodies Levels of serum TSHR-blocking antibodies (TBAb) were measured according to the manufacturer’s (Quidel, San Diego, USA) instructions for the CE-marked cell-based bioassay [ 27

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000508790
Volume/Issue:
Volume 9: Issue 1_Suppl
Free access
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

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000478522
Volume/Issue:
Volume 6: Issue 5
Free access
George J. Kahaly Johannes Gutenberg University Medical Center, Mainz, Germany

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either via competitive-binding immunoassays or with bioassays [ 4 ]. Antibody-binding assays only report the presence or absence of TSHR-Ab and their concentrations, but do not indicate their functional activity. Bioassays, in contrast, indicate whether

Article Type:
Editorial
DOI:
https://doi.org/10.1159/000375445
Volume/Issue:
Volume 4: Issue 1
Free access
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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; however, it is still unclear whether the development of optic nerve compression can be prevented or treated with this new drug. In addition, we need to find out if directly targeting the TSHR with blocking antibodies or small-molecule antagonists is even

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000511871
Volume/Issue:
Volume 9: Issue 1_Suppl
Free access
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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hyperthyroidism with resultant hypothyroidism. Thyroid-stimulating antibodies, the proximal cause of Graves hyperthyroidism, arise from the breakdown in self-tolerance to the TSHR [ 11 ]. The pathophysiological relationship between TSHR, TPO, and Tg autoantibodies

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000488079
Volume/Issue:
Volume 7: Issue 3
Free access
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

Article Type:
Case Report
DOI:
https://doi.org/10.1159/000338038
Volume/Issue:
Volume 1: Issue 2
Free access
Naohiro Araki Diagnostic Division, Otsuka Pharmaceutical Co. Ltd., Tokushima, Japan

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Mitsuru Iida Diagnostic Division, Otsuka Pharmaceutical Co. Ltd., Tokushima, Japan

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Nobuyuki Amino Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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Shinji Morita Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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Akane Ide Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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Eijun Nishihara Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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Mitsuru Ito Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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Jun Saito Department of Medicine, Yokohama Rosai Hospital, Yokohama, Japan

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Tetsuo Nishikawa Department of Medicine, Yokohama Rosai Hospital, Yokohama, Japan

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Kiyonori Katsuragi Diagnostic Division, Otsuka Pharmaceutical Co. Ltd., Tokushima, Japan

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Akira Miyauchi Department of Internal Medicine, Kuma Hospital, Kobe, Japan

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either thyroid-stimulating antibodies (TSAb) or thyroid-stimulating blocking antibodies (TSBAb). TSAb have been shown to be responsible for hyperthyroidism in Graves' disease (GD), whereas TSBAb occur mainly in patients with atrophic thyroiditis and

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000371740
Volume/Issue:
Volume 4: Issue 1
Open access
R. Paschke Department of Endocrinology and Nephrology, Leipzig University, Leipzig, Germany

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M. Niedziela Department of Pediatric Endocrinology and Rheumatology, Poznan University of Medical Sciences, Poznan, Poland

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B. Vaidya Department of Endocrinology, Royal Devon and Exeter Hospital, Peninsula Medical School, Exeter, UK

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L. Persani Department of Clinical Sciences, and Community Health, University of Milan, and Istituto Auxologico Italiano, Milan, Italy

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B. Rapoport Autoimmune Disease Unit, Cedars-Sinai Research Institute and School of Medicine, University of California, Los Angeles, Calif., USA

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J. Leclere Centre Hospitalier Universitaire de Nancy, Nancy, France

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characterized by: (1) A positive family history of non-autoimmune hyperthyroidism with dominant inheritance. (2) An absence of clinical (ophthalmopathy or dermopathy) or other stigmata of autoimmunity [TSHR antibodies, thyroid peroxidase (TPO) antibodies

Article Type:
Guideline
DOI:
https://doi.org/10.1159/000342982
Volume/Issue:
Volume 1: Issue 3
Free access
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

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000504509
Volume/Issue:
Volume 9: Issue 2
Free access