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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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molecule IGF-1R inhibitor, linsitinib, inhibited HA stimulation by TSH [ 6 ]; (2) the high-potency phase of the biphasic dose response of HA secretion stimulated by a monoclonal TSHR-stimulating antibody (TSAb) M22, which was derived from a patient with

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000511538
Volume/Issue:
Volume 9: Issue 1_Suppl
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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]. Pathological activation of the TSHR by TSHR-stimulating autoimmune antibodies (TSAb) leads to the uncontrolled production of thyroid hormones T3 and T4 in the thyroid causing hyperthyroidism in Graves’ disease (GD) [ 5 ]. The TSAb binds to the TSHR at a similar

Article Type:
Review Article
DOI:
https://doi.org/10.1159/000511871
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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, 28 ]. The cut-off is at 34% inhibition. All sera were measured in duplicate and data were reported as mean values. Bioassay for Stimulating TSHR Antibodies Levels of serum TSHR-stimulating antibodies (TSAb) were measured with an FDA

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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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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receptors per cell. In contrast, studies with the stimulating human monoclonal antibody (M22) [ 39 ] allow for comparison of the signal transduction of the two TSH-R. When stimulating with M22 MAb, the CHO-MC4 cells produced higher levels of cAMP and

Article Type:
Research Article
DOI:
https://doi.org/10.1159/000504509
Volume/Issue:
Volume 9: Issue 2
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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
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
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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Hashimoto's thyroiditis [ 3 ]. The amount of TSHR antibodies can be measured with competitive binding assays, the so-called thyrotropin-binding inhibitory immunoglobulin/TSHR antibodies (TRAb) assay, using either labeled thyroid-stimulating hormone (TSH

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