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Artykuły w czasopismach na temat „TSH receptor autoantibodies”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Michalek, Krzysztof, Syed A. Morshed, Rauf Latif, and Terry F. Davies. "TSH receptor autoantibodies." Autoimmunity Reviews 9, no. 2 (2009): 113–16. http://dx.doi.org/10.1016/j.autrev.2009.03.012.

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Sanders, Jane, Yasuo Oda, Sara Roberts, et al. "The Interaction of TSH Receptor Autoantibodies with 125I-Labelled TSH Receptor." Journal of Clinical Endocrinology & Metabolism 84, no. 10 (1999): 3797–802. http://dx.doi.org/10.1210/jcem.84.10.6071.

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Abstract Detergent-solubilized porcine TSH receptor (TSHR) has been labeled with 125I using a monoclonal antibody to the C-terminal domain of the receptor. The ability of sera containing TSHR autoantibody to immunoprecipitate the labeled receptor was then investigated. Sera negative for TSHR autoantibody (as judged by assays based on inhibition of labeled TSH binding to detergent-solubilized porcine TSHR) immunoprecipitated about 4% of the labeled receptor, whereas sera with high levels of receptor autoantibody immunoprecipitated more than 25% of the labeled receptor. The ability to immunoprec

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3

Furmaniak, J., Y. Nakajima, F. A. Hashim, et al. "The TSH receptor: Structure and interaction with autoantibodies in thyroid disease." Acta Endocrinologica 116, no. 1_Suppl (1987): S157—S165. http://dx.doi.org/10.1530/acta.0.114s157.

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Abstract. Studies of the TSH receptor using affinity labelling with photoactive derivatives of TSH and analysis by SDS-PAGE have shown that the receptor contains 2 subunits (A and B), linked by a disulphide bridge. Similar results are obtained with TSH receptors from human, porcine and guinea pig thyroid tissue and from guinea pig fat. Analysis of affinity labelled receptors under non-denaturing conditions suggest that subunits additional to the A and B subunits are not present. Hydrodynamic measurements indicate that the receptor A subunit has an approximately spherical structure (Stokes' rad

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4

Zakarija, M., and J. M. McKenzie. "Autoantibodies to the TSH Receptor." Experimental and Clinical Endocrinology & Diabetes 97, no. 02/03 (2009): 165–69. http://dx.doi.org/10.1055/s-0029-1211057.

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Huang, G. C., K. S. Collison, A. M. McGregor, and J. P. Banga. "Expression of a human thyrotrophin receptor fragment in Escherichia coli and its interaction with the hormone and autoantibodies from patients with Graves' disease." Journal of Molecular Endocrinology 8, no. 2 (1992): 137–44. http://dx.doi.org/10.1677/jme.0.0080137.

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ABSTRACT Graves' disease is an autoimmune thyroid disease characterized by the presence of pathogenic autoantibodies to the TSH receptor (TSH-R). By using polymerase chain reaction, the extracellular region of the human TSH-R cDNA has been amplified and used to prepare recombinant TSH-R (extracellular) protein fused with glutathione-S-transferase (GST). Purification of the recombinant TSH-R (extracellular)-GST fusion protein was achieved by preparative gel electrophoresis in SDS or by preparative isoelectric focusing in urea. Following removal of SDS by detergent exchange or urea by dialysis,

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6

Furmaniak, J., J. Sanders, P. Sanders, J. Miller-Gallacher, M. M. Ryder, and B. Rees Smith. "Practical applications of studies on the TSH receptor and TSH receptor autoantibodies." Endocrine 68, no. 2 (2020): 261–64. http://dx.doi.org/10.1007/s12020-019-02180-9.

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Kakinuma, Ayumu, Gregorio D. Chazenbalk, Juan Carlos Jaume, Basil Rapoport, and Sandra M. McLachlan. "The Human Thyrotropin (TSH) Receptor in a TSH Binding Inhibition Assay for TSH Receptor Autoantibodies1." Journal of Clinical Endocrinology & Metabolism 82, no. 7 (1997): 2129–34. http://dx.doi.org/10.1210/jcem.82.7.4092.

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Seven years after the molecular cloning of the human TSH receptor (TSHR), the porcine TSHR remains in general use in the TSH binding inhibition (TBI) assay for autoantibodies to the TSHR. We compared porcine and recombinant human TSHR in two types of TBI assays: one using intact Chinese hamster ovary cells expressing the recombinant human TSHR on their surface, and the other using soluble receptors extracted from these cells with detergent. In the intact cell TBI assay, monolayers expressing large numbers of TSHR were less effective than cells expressing few receptors. These findings are consi

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8

Kakinuma, A. "The Human Thyrotropin (TSH) Receptor in a TSH Binding Inhibition Assay for TSH Receptor Autoantibodies." Journal of Clinical Endocrinology & Metabolism 82, no. 7 (1997): 2129–34. http://dx.doi.org/10.1210/jc.82.7.2129.

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9

Lytton, Simon D., and George J. Kahaly. "Bioassays for TSH-receptor autoantibodies: An update." Autoimmunity Reviews 10, no. 2 (2010): 116–22. http://dx.doi.org/10.1016/j.autrev.2010.08.018.

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10

Vlase, H., N. Matsuoka, P. N. Graves, R. P. Magnusson, and T. F. Davies. "Folding-Dependent Binding of Thyrotropin (TSH) and TSH Receptor Autoantibodies to the Murine TSH Receptor Ectodomain*." Endocrinology 138, no. 4 (1997): 1658–66. http://dx.doi.org/10.1210/endo.138.4.5037.

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11

Davies Jones, E., F. A. Hashim, Y. Kajita, et al. "Interaction of autoantibodies to thyrotropin receptor with a hydrophilic subunit of the thyrotropin receptor." Biochemical Journal 228, no. 1 (1985): 111–17. http://dx.doi.org/10.1042/bj2280111.

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Reduction of human thyroid membranes with dithiothreitol caused the release of a water-soluble glycoprotein which neutralized the thyrotropin (TSH) receptor-binding and thyroid-stimulating activities of Graves‘ serum. Analysis of the protein by gel filtration and sucrose density gradient centrifugation allowed estimates of 3.45 nm for the Stokes’ radius, 3.6 S for the s20,w and 47 000 +/- 5000 (mean +/- S.D.; n = 4) for the Mr. The material released by dithiothreitol treatment could be crosslinked to 125I-labelled TSH coupled to N-hydroxysuccinimidyl 4-azidobenzoate (125I-HSAB-TSH), suggesting

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12

Huang, G. C., M. J. Page, L. B. Nicholson, K. S. Collison, A. M. McGregor, and J. P. Banga. "The thyrotrophin hormone receptor of Graves' disease: overexpression of the extracellular domain in insect cells using recombinant baculovirus, immunoaffinity purification and analysis of autoantibody binding." Journal of Molecular Endocrinology 10, no. 2 (1993): 127–42. http://dx.doi.org/10.1677/jme.0.0100127.

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ABSTRACT Since the cloning of the TSH receptor (TSH-R), the target autoantigen of Graves' disease, the receptor has been expressed in a variety of eukaryotic cells to obtain a functional molecule. Despite this success, the levels of receptor expression have been marginally higher than the extremely low levels found in thyroid cells, preventing any progress on the purification of the molecule. In this study, the large extracellular region of the TSH-R, without the membrane spanning segments, has been expressed in insect cells using recombinant baculovirus to generate substantial quantities of t

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13

Rapoport, B. "The Thyrotropin (TSH)-Releasing Hormone Receptor: Interaction with TSH and Autoantibodies." Endocrine Reviews 19, no. 6 (1998): 673–716. http://dx.doi.org/10.1210/er.19.6.673.

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14

Rapoport, Basil, Gregorio D. Chazenbalk, Juan Carlos Jaume, and Sandra M. McLachlan. "The Thyrotropin (TSH)-Releasing Hormone Receptor: Interaction with TSH and Autoantibodies*." Endocrine Reviews 19, no. 6 (1998): 673–716. http://dx.doi.org/10.1210/edrv.19.6.0352.

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15

Byfield, P. G. H., S. C. Davies, S. Copping, F. E. Barclay, and S. P. Borriello. "Thyrotrophin (TSH)-binding proteins in bacteria and their cross-reaction with autoantibodies against the human TSH receptor." Journal of Endocrinology 121, no. 3 (1989): 571–77. http://dx.doi.org/10.1677/joe.0.1210571.

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ABSTRACT A screen of a range of bacteria normally found in gut flora identified eight with the ability to bind TSH specifically. These included the previously reported Yersinia enterocolitica, Gram-positive, Gramnegative, pathogenic and commensal organisms. Eleven preparations of TSH-receptor autoantibodies strongly able to displace 125I-labelled TSH from the mammalian TSH receptor differed in their ability to displace the tracer from binding to bacterial extracts. None could displace the tracer from E. coli 06–1, four displaced 125I-labelled TSH from E. coli V21/1 and five displaced the trace

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16

Derkach, K. V., A. A. Bakhtyukov, V. N. Sorokoumov, I. A. Lebedev, E. A. Didenko, and A. O. Shpakov. "Low molecular inverse agonist of the thyrotropin receptor is active both intraperitoneal and oral administration." Российский физиологический журнал им И М Сеченова 110, no. 1 (2024): 108–21. http://dx.doi.org/10.31857/s0869813924010078.

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Autoimmune hyperthyroidism (Graves’ disease), which is caused by stimulating autoantibodies to the thyroid-stimulating hormone (TSH) receptor, and thyroid gland (TG) tumors, caused by constitutively increased activity of this receptor, are widespread and have a poor prognosis. The drugs used to treat them are not very effective and have many side effects. One of the approaches for the treatment of these thyroid diseases may be the use of allosteric regulators of the TSH receptor with the activity of inverse agonists. The purpose of the work was to study the effects of our previously developed

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17

Tonacchera, Massimo, Sabine Costagliola, Filomena Cetani, et al. "Patient with monoclonal gammopathy, thyrotoxicosis, pretibial myxedema and thyroid-associated ophthalmopathy; demonstration of direct binding of autoantibodies to the thyrotropin receptor." European Journal of Endocrinology 134, no. 1 (1996): 97–103. http://dx.doi.org/10.1530/eje.0.1340097.

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Tonacchera M. Costagliola S, Cetani F, Ducobu J. Stordeur P. Vassart G. Ludgate M. Patient with monoclonal gammopathy, thyrotoxicosis, pretibial myxedema and thyroid-associated ophthalmopathy: demonstration of direct binding of autoantibodies to the thyrotropin receptor. Eur J Endocrinol 1996:134:97–103. ISSN 0804–4643 We describe a patient with monoclonal gammopathy who subsequently developed thyrotoxicosis, pretibial myxedema and thyroid-associated ophthalmopathy. The pathogenesis of thyrotoxicosis in Graves' disease is due to the presence of autoantibodies that mimic the action of thyrotrop

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18

Leedman, Peter J., Paul J. Harrison, and Leonard C. Harrison. "Immunoblotting for the detection of TSH receptor autoantibodies." Journal of Autoimmunity 4, no. 3 (1991): 529–42. http://dx.doi.org/10.1016/0896-8411(91)90164-8.

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19

Ochi, Y., T. Nagamune, Y. Nakajima, et al. "Anti-TSH antibodies in Graves' disease and their failure to interact with TSH receptor antibodies." Acta Endocrinologica 120, no. 6 (1989): 773–77. http://dx.doi.org/10.1530/acta.0.1200773.

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Abstract. The occasional occurrence in sera of patients with Graves' disease of negative values in the assay for TSH receptor antibodies led to the discovery of endogenous antibodies to TSH. We examined the sera of approximately 2500 patients with Graves' disease. Eight positive sera were found. The IgG in all 8 sera showed higher binding with both bTSH and porcine TSH (pTSH) than with human TSH (hTSH). This means that autoantibodies to TSH in sera from patients with Graves' disease are rare and often directed towards heterologous bovine and porcine TSH. When hTSH levels were determined in ser

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20

Fokina, E. F., and A. O. Shpakov. "Thyroid-Stimulating Hormone Receptor: the Role in the Development of Thyroid Pathology and Its Correction." Journal of Evolutionary Biochemistry and Physiology 58, no. 5 (2022): 1439–54. http://dx.doi.org/10.1134/s0022093022050143.

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Abstract One of the key elements responsible for the thyroid response to thyroid-stimulating hormone (TSH) is the TSH receptor (TSHR), which belongs to the G protein-coupled receptor superfamily. Binding of TSH or stimulatory autoantibodies to the TSHR extracellular domain triggers multiple signaling pathways in target cells that are mediated through various types of G proteins and β-arrestins. Inhibitory autoantibodies, in contrast, suppress TSHR activity, inducing hypothyroid states. Activating mutations lead to constitutively active TSHR forms and can trigger cancer. Therefore, the TSHR is

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21

Gerges, Monica M., Mohamed A. El-Desouky, Osama E. Shalaby, and Reham R. Shabana. "Role of thyroid antibodies in the diagnosis of thyroid eye disease." Tanta Medical Journal 53, no. 2 (2025): 198–205. https://doi.org/10.4103/tmj.tmj_73_24.

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Background Thyroid eye disease (TED) is an autoimmune disorder caused by autoantibodies targeting thyroid-stimulating hormone (TSH) receptors. Aim To correlate the clinical profile of TED with the level of circulating biomarkers [TSH receptor antibody and antithyroglobulin antibody (anti-TgAb)]. Patients and methods A prospective observational cross-sectional study carried out on 40 TED patients. The patients were subjected to full history taking, endocrinological evaluation, and full ophthalmological examination. All the participants underwent thyroid function tests (TSH, free T3, and free T4

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22

Mellow, Prettysun Ang. "GRAVES DISEASE." Jurnal Widya Medika 9, no. 1 (2023): 66–78. http://dx.doi.org/10.33508/jwm.v9i1.4510.

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Graves' disease is one of the most common autoimmune diseases. The disease is named after the scientist Robert James Graves, who first described it in the 19th century as a syndrome with an enlarged and overactive thyroid gland (hyperthyroidism due to circulating autoantibodies), rapid heart rate, and eye abnormalities. graves’ disease is the most common cause of hyperthyroidism and affects more women than men. Graves’ disease can appear at any age, but it most commonly appears for the first time between the ages of 20 and 40. Factor is a predisposition that is more dominant than environmental

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23

Sellschopp, Ch, M. Derwahl, H. Schaube, J. Seifert, and H. Hamelmann. "Direct immunostaining of TSH receptor related autoantibodies in Graves' disease." Acta Endocrinologica 114, no. 1 (1987): 132–37. http://dx.doi.org/10.1530/acta.0.1140132.

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Abstract. Ten thyroid specimens from patients with Graves' disease were investigated immunohistologically with respect to the localisation of thyrotropin (TSH) receptor related autoantibodies. After conventional preparation of formalin-fixed and paraffin-embedded thyroid slices for immunostaining, 3–5 μm tissue sections were incubated with a porcine thyrotropin receptor containing membrane preparation (pTSH-R). The TSH receptor containing membrane fragments bound to the thyroid tissue were revealed with a slightly modified unlabelled PAP technique according to Sternberger, using an antiserum t

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Marques, Pedro, Karim Chikh, Anne Charrié, Rosa Pina, Maria João Bugalho, and Lurdes Lopes. "Hipotiroidismo Associado a Anticorpos Anti-Receptor da Hormona TSH com Ação Bloqueadora Determinada In Vitro." Acta Médica Portuguesa 28, no. 5 (2015): 663. http://dx.doi.org/10.20344/amp.6521.

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Thyroid-stimulating hormone-receptor autoantibodies normally causes hyperthyroidism. However, they might have blocking activity causing hypothyroidism. A 11-year-old girl followed due to type 1 diabetes mellitus, celiac disease and euthyroid lymphocytic thyroiditis at diagnosis. Two years after the initial evaluation, thyroid-stimulating hormone was suppressed with normal free T4; nine months later, a biochemical evolution to hypothyroidism with thyroid-stimulating hormone-receptor autoantibodies elevation was seen; the patient remained always asymptomatic. Chinese hamster ovary cells were tra

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Núñez Miguel, Ricardo, Jane Sanders, Paul Sanders, et al. "Similarities and differences in interactions of thyroid stimulating and blocking autoantibodies with the TSH receptor." Journal of Molecular Endocrinology 49, no. 2 (2012): 137–51. http://dx.doi.org/10.1530/jme-12-0040.

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Binding of a new thyroid-stimulating human monoclonal autoantibody (MAb) K1–18 to the TSH receptor (TSHR) leucine-rich domain (LRD) was predicted using charge–charge interaction mapping based on unique complementarities between the TSHR in interactions with the thyroid-stimulating human MAb M22 or the thyroid-blocking human MAb K1–70. The interactions of K1–18 with the TSHR LRD were compared with the interactions in the crystal structures of the M22–TSHR LRD and K1–70–TSHR LRD complexes. Furthermore, the predicted position of K1–18 on the TSHR was validated by the effects of TSHR mutations on

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26

Minich, Waldemar B., Cornelia Lenzner, Andreas Bergmann, and Nils G. Morgenthaler. "A Coated Tube Assay for the Detection of Blocking Thyrotropin Receptor Autoantibodies." Journal of Clinical Endocrinology & Metabolism 89, no. 1 (2004): 352–56. http://dx.doi.org/10.1210/jc.2003-030823.

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We developed a coated tube assay to discriminate TSH-receptor-stimulating autoantibodies [thyroid-stimulating antibodies (TSAb)] from those autoantibodies blocking TSH binding without intrinsic activation [thyroid-blocking antibodies (TBAb)]. The wild-type TSH receptor in the TSH binding-inhibitory assay was exchanged for a chimeric receptor where a TSAb epitope (amino acids 8–165) was replaced by comparable LH-R residues. Binding of 125I-labeled TSH to this chimera could be inhibited by sera containing TBAb up to 95%. Sera from 316 patients with Graves’ disease and 17 with autoimmune thyroid

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Daminov, Abdurasul Taxirovich, Quvondiq Rayimov, Temurbek G`aybullayev, Vosidbek Vohidov, and Dilorom Omonova. "PREGNANT WOMAN WITH DIFFUSE TOXIC GOITRE." Research and implementation 2, no. 4 (2024): 197–205. https://doi.org/10.5281/zenodo.10884673.

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The influence of diffuse toxic goiter on the course and outcome of pregnancy was studied. 67 pregnant women with diffuse toxic goiter were examined. The comparison group consisted of 38 pregnant women without thyroid pathology. The examination included determination of free thyroxine, TSH, autoantibodies to the TSH receptor and thyroid peroxidase in the blood of pregnant women and umbilical cord blood, as well as ultrasound of the thyroid gland of newborns and the TSH/free ratio. T4. In women with unresolved thyrotoxicosis, pregnancy and childbirth were more often complicated by the threat of

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FILETTI, S., D. FOTI, G. COSTANTE, and B. RAPOPORT. "Recombinant Human Thyrotropin (TSH) Receptor in a Radioreceptor Assay for the Measurement of TSH Receptor Autoantibodies*." Journal of Clinical Endocrinology & Metabolism 72, no. 5 (1991): 1096–101. http://dx.doi.org/10.1210/jcem-72-5-1096.

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Rootwelt, K. "Evaluation of a radioreceptor assay for TSH receptor autoantibodies." Scandinavian Journal of Clinical and Laboratory Investigation 48, no. 2 (1988): 157–64. http://dx.doi.org/10.3109/00365518809085408.

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Nagayama, Y., H. L. Wadsworth, D. Russo, G. D. Chazenbalk, and B. Rapoport. "Binding domains of stimulatory and inhibitory thyrotropin (TSH) receptor autoantibodies determined with chimeric TSH-lutropin/chorionic gonadotropin receptors." Journal of Clinical Investigation 88, no. 1 (1991): 336–40. http://dx.doi.org/10.1172/jci115297.

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Krieger, Christine C., Robert F. Place, Carmine Bevilacqua, et al. "TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis." Journal of Clinical Endocrinology & Metabolism 101, no. 6 (2016): 2340–47. http://dx.doi.org/10.1210/jc.2016-1315.

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Abstract Context: The TSH receptor (TSHR) is considered the main target of stimulatory autoantibodies in the pathogenesis of Graves' ophthalmopathy (GO); however, it has been suggested that stimulatory IGF-1 receptor (IGF-1R) autoantibodies also play a role. Objective: We previously demonstrated that a monoclonal stimulatory TSHR antibody, M22, activates TSHR/IGF-1R cross talk in orbital fibroblasts/preadipocytes obtained from patients with GO (GO fibroblasts [GOFs]). We show that cross talk between TSHR and IGF-1R, not direct IGF-1R activation, is involved in the mediation of GO pathogenesis

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Christensen, Niels Juel, Gurli Habekost, and Palle Bratholm. "Decrease in TSH Receptor Autoantibodies during Antithyroid Treatment: Relationship with a Long Noncoding Heg RNA and Cdk1 mRNA in Mononuclear Cells." ISRN Endocrinology 2011 (July 6, 2011): 1–4. http://dx.doi.org/10.5402/2011/287052.

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We have previously shown that a long noncoding RNA transcript Heg is negatively correlated with TSH receptor autoantibodies (TRAb) in patients with untreated Graves' disease and with CD14 mRNA in treated patients and controls. Thus patients with high concentrations of Heg RNA have low levels of TRAb or CD14 mRNA, respectively. Here we show that an additional factor, gene expression of Cdk1 in mononuclear cells, is positively related to concentrations of TRAb in patients with untreated Graves' disease. Cdk1 mRNA is very important for regulation of cell cycle activity. It is well known that TRAb

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Hotta, Asami, Tomohiro Tanaka, Haruka Kato, et al. "A Case of Euthyroid Graves’ Ophthalmopathy in a Patient Sero-Negative for TSH Receptor Autoantibody." Case Reports in Endocrinology 2018 (June 13, 2018): 1–6. http://dx.doi.org/10.1155/2018/1707959.

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We report of a case of Graves’ ophthalmopathy presented solely with symptoms of the eyes with normal thyroid function tests and negative immunoreactive TSH receptor autoantibody. 40-year-old male was referred to our hospital due to 2-month history of ocular focusing deficit without any signs or symptoms of hyper- or hypothyroidism. Serum thyroid function tests and 99mTc uptake were both within the normal range. Anti-thyroid autoantibodies were all negative except for the cell-based assay for serum TSH receptor stimulating activity. Since orbital CT scan and MRI gave typical results compatible

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Laurberg, Peter, Birte Nygaard, Stig Andersen, et al. "Association between TSH-Receptor Autoimmunity, Hyperthyroidism, Goitre, and Orbitopathy in 208 Patients Included in the Remission Induction and Sustenance in Graves’ Disease Study." Journal of Thyroid Research 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/165487.

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Background. Graves’ disease may have a number of clinical manifestations with varying degrees of activity that may not always run in parallel.Objectives. To study associations between serum levels of TSH-receptor autoantibodies and the three main manifestations of Graves’ disease (hyperthyroidism, goiter, and presence of orbitopathy) at the time of diagnosis of hyperthyroidism.Methods. We describe a cohort of 208 patients with newly diagnosed Graves’ hyperthyroidism. Patients were enrolled in a multiphase study of antithyroid drug therapy of Graves’ hyperthyroidism, entitled “Remission Inducti

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35

Lee, Michelle N., and Jeffrey A. Colburn. "A Grave Turn on Hashimoto’s Thyroiditis - A Case Series on Four Patients With Autoimmune Hypothyroidism that Converted to Grave’s Disease." Journal of the Endocrine Society 5, Supplement_1 (2021): A913—A914. http://dx.doi.org/10.1210/jendso/bvab048.1865.

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Abstract Disclaimer: The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. Government. Introduction: The most common cause of hypothyroidism is Hashimoto’s thyroiditis, a destructive autoimmune injury to the thyroid gland. Rarely, autoimmune hypothyroidism can be caused by thyroid-stimulating hormone (TSH) receptor blocking antibodie

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Prentice, Louise, Jane F. Sanders, Maria Perez, et al. "Thyrotropin (TSH) Receptor Autoantibodies Do Not Appear to Bind to the TSH Receptor Produced in anin VitroTranscription/Translation System." Journal of Clinical Endocrinology & Metabolism 82, no. 4 (1997): 1288–92. http://dx.doi.org/10.1210/jcem.82.4.3895.

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Jaume, Juan Carlos, Ayumu Kakinuma, Gregorio D. Chazenbalk, Basil Rapoport, and Sandra M. McLachlan. "Thyrotropin Receptor Autoantibodies in Serum Are Present at Much Lower Levels Than Thyroid Peroxidase Autoantibodies: Analysis by Flow Cytometry*." Journal of Clinical Endocrinology & Metabolism 82, no. 2 (1997): 500–507. http://dx.doi.org/10.1210/jcem.82.2.3740.

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Abstract Using Chinese hamster ovary (CHO) cells that express high numbers of TSH receptor (TSHR) on their surface, we studied the feasibility of detecting directly by flow cytometry the binding of autoantibodies in patients’ sera to the native TSHR. After using a serum (BBl) with high potency in the TSH binding inhibition (TBI) assay to establish the protocol, we studied an additional 38 sera: 10 without TBI activity (1–4.2% inhibition), 10 with moderately high TBI values (17.3–39.4% inhibition), 10 with high TBI levels (52–95.1% inhibition), 4 from normal individuals without autoimmune thyro

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Mcgregor, Alan M. "Autoantibodies To The Tsh Receptor In Patients With Autoimmune Thyroid Disease." Clinical Endocrinology 33, no. 6 (1990): 683–85. http://dx.doi.org/10.1111/j.1365-2265.1990.tb03905.x.

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Haider, Y. Abdulrazaq. "Evaluation of Thyroperoxidase and TSH Receptor Autoantibodies in Thyroid Dysfunction Patients." INTERNATIONAL JOURNAL OF MEDICAL SCIENCE AND CLINICAL RESEARCH STUDIES 03, no. 09 (2023): 1831–34. https://doi.org/10.5281/zenodo.8321536.

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Thyroid autoimmune disease is one of the most common disorders which are generally associated with existence of anti-thyroid peroxidase (TPO) in addition to ant thyroid stimulating hormone receptor (TSHR) antibodies, and anti-thyroglobulin (Tg). The present study was a cross-sectional one, conducted on (200) patients selected randomly from cases already diagnosed with thyroid disorder diseases by a specialized endocrinology center in AL-Basra city / Iraq. Where TPO test was performed for 127 of them, and TRAB test was conducted for the remaining 73 patients. The study showed that 74% of the ca

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Chen, Chun-Rong, Pavel Pichurin, Gregorio D. Chazenbalk, et al. "Low-Dose Immunization with Adenovirus Expressing the Thyroid-Stimulating Hormone Receptor A-Subunit Deviates the Antibody Response toward That of Autoantibodies in Human Graves’ Disease." Endocrinology 145, no. 1 (2004): 228–33. http://dx.doi.org/10.1210/en.2003-1134.

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Abstract Immunization with adenovirus expressing the TSH receptor (TSHR) induces hyperthyroidism in 25–50% of mice. Even more effective is immunization with a TSHR A-subunit adenovirus (65–84% hyperthyroidism). Nevertheless, TSHR antibody characteristics in these mice do not mimic accurately those of autoantibodies in typical Graves’ patients, with a marked TSH-blocking antibody response. We hypothesized that this suboptimal antibody response was consequent to the standard dose of TSHR-adenovirus providing too great an immune stimulus. To test this hypothesis, we compared BALB/c mice immunized

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Miller-Gallacher, Jennifer, Paul Sanders, Stuart Young, et al. "Crystal structure of a ligand-free stable TSH receptor leucine-rich repeat domain." Journal of Molecular Endocrinology 62, no. 3 (2019): 117–28. http://dx.doi.org/10.1530/jme-18-0213.

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The crystal structures of the thyroid-stimulating hormone receptor (TSHR) leucine-rich repeat domain (amino acids 22–260; TSHR260) in complex with a stimulating human monoclonal autoantibody (M22TM) and in complex with a blocking human autoantibody (K1-70™) have been solved. However, attempts to purify and crystallise free TSHR260, that is not bound to an autoantibody, have been unsuccessful due to the poor stability of free TSHR260. We now describe a TSHR260 mutant that has been stabilised by the introduction of six mutations (H63C, R112P, D143P, D151E, V169R and I253R) to form TSHR260-JMG55T

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López Ortega, José María, Pilar Salvador Martínez, Delia Acevedo-León, and Núria Estañ Capell. "Anti-TSH receptor antibodies (TRAb): Comparison of two third generation automated immunoassays broadly used in clinical laboratories and results interpretation." PLOS ONE 17, no. 7 (2022): e0270890. http://dx.doi.org/10.1371/journal.pone.0270890.

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Graves’ disease (GD) is the most common cause of hyperthyroidism in iodine-replete populations. It is an autoimmune disease caused by autoantibodies to the TSHR (TRAb). Although the diagnostic is mainly clinical, measuring TRAb improves accuracy and provides valuable prognostic information. The aim of this study was to compare the performance of two of the most widely used immunoassays i.e., EliA™ anti-TSH-R and Elecsys® anti-TSH-R. We have carried out a comparative study measuring TRAb by the two immunoassays in consecutive sera samples referred to the laboratory for TRAb measurement. Autoant

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Vargas-Uricoechea, Hernando. "Molecular Mechanisms in Autoimmune Thyroid Disease." Cells 12, no. 6 (2023): 918. http://dx.doi.org/10.3390/cells12060918.

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The most common cause of acquired thyroid dysfunction is autoimmune thyroid disease, which is an organ-specific autoimmune disease with two presentation phenotypes: hyperthyroidism (Graves-Basedow disease) and hypothyroidism (Hashimoto’s thyroiditis). Hashimoto’s thyroiditis is distinguished by the presence of autoantibodies against thyroid peroxidase and thyroglobulin. Meanwhile, autoantibodies against the TSH receptor have been found in Graves-Basedow disease. Numerous susceptibility genes, as well as epigenetic and environmental factors, contribute to the pathogenesis of both diseases. This

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Costagliola, S., L. Alcalde, M. Tonacchera, J. Ruf, G. Vassart, and M. Ludgate. "Induction of Thyrotropin Receptor (TSH-R) Autoantibodies and Thyroiditis in Mice Immunized with the Recombinant TSH-R." Biochemical and Biophysical Research Communications 199, no. 2 (1994): 1027–34. http://dx.doi.org/10.1006/bbrc.1994.1332.

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Krieger, Christine C., Susanne Neumann, and Marvin C. Gershengorn. "Is There Evidence for IGF1R-Stimulating Abs in Graves’ Orbitopathy Pathogenesis?" International Journal of Molecular Sciences 21, no. 18 (2020): 6561. http://dx.doi.org/10.3390/ijms21186561.

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In this review, we summarize the evidence against direct stimulation of insulin-like growth factor 1 receptors (IGF1Rs) by autoantibodies in Graves’ orbitopathy (GO) pathogenesis. We describe a model of thyroid-stimulating hormone (TSH) receptor (TSHR)/IGF1R crosstalk and present evidence that observations indicating IGF1R’s role in GO could be explained by this mechanism. We evaluate the evidence for and against IGF1R as a direct target of stimulating IGF1R antibodies (IGF1RAbs) and conclude that GO pathogenesis does not involve directly stimulating IGF1RAbs. We further conclude that the prep

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Morgenthaler, Nils G., Waldemar B. Minich, Marita Willnich, et al. "Affinity purification and diagnostic use of TSH receptor autoantibodies from human serum." Molecular and Cellular Endocrinology 212, no. 1-2 (2003): 73–79. http://dx.doi.org/10.1016/j.mce.2003.09.018.

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Aliesky, Holly, Cynthia L. Courtney, Basil Rapoport, and Sandra M. McLachlan. "Thyroid Autoantibodies Are Rare in Nonhuman Great Apes and Hypothyroidism Cannot Be Attributed to Thyroid Autoimmunity." Endocrinology 154, no. 12 (2013): 4896–907. http://dx.doi.org/10.1210/en.2013-1717.

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The great apes include, in addition to Homo, the genera Pongo (orangutans), Gorilla (gorillas), and Pan, the latter comprising two species, P. troglodytes (chimpanzees) and P. paniscus (bonobos). Adult-onset hypothyroidism was previously reported in 4 individual nonhuman great apes. However, there is scarce information on normal serum thyroid hormone levels and virtually no data for thyroid autoantibodies in these animals. Therefore, we examined thyroid hormone levels and TSH in all nonhuman great ape genera including adults, adolescents, and infants. Because hypothyroidism in humans is common

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Núñez Miguel, R., J. Sanders, D. Y. Chirgadze, J. Furmaniak, and B. Rees Smith. "Thyroid stimulating autoantibody M22 mimics TSH binding to the TSH receptor leucine rich domain: a comparative structural study of protein–protein interactions." Journal of Molecular Endocrinology 42, no. 5 (2009): 381–95. http://dx.doi.org/10.1677/jme-08-0152.

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The TSH receptor (TSHR) ligands M22 (a thyroid stimulating human monoclonal antibody) and TSH, bind to the concave surface of the leucine rich repeats domain (LRD) of the TSHR and here, we show that M22 mimics closely the binding of TSH. We compared interactions produced by M22 with the TSHR in the M22–TSHR crystal structure (2.55 Å resolution) and produced by TSH with the TSHR in a TSH–TSHR comparative model. The crystal structure of the TSHR and a comparative model of TSH based on the crystal structure of FSH were used as components to build the TSH–TSHR model. This model was built based on

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Balucan, Francis S., Syed A. Morshed, and Terry F. Davies. "Thyroid Autoantibodies in Pregnancy: Their Role, Regulation and Clinical Relevance." Journal of Thyroid Research 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/182472.

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Autoantibodies to thyroglobulin and thyroid peroxidase are common in the euthyroid population and are considered secondary responses and indicative of thyroid inflammation. By contrast, autoantibodies to the TSH receptor are unique to patients with Graves' disease and to some patients with Hashimoto's thyroiditis. Both types of thyroid antibodies are useful clinical markers of autoimmune thyroid disease and are profoundly influenced by the immune suppression of pregnancy and the resulting loss of such suppression in the postpartum period. Here, we review these three types of thyroid antibodies

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Takei, Masahiro, Hiroaki Ishii, Yoshihiko Sato, and Mitsuhisa Komatsu. "A Case of Marine-Lenhart Syndrome with a Negative TSH Receptor Antibody Titer Successfully Treated with a Fixed, Low Dose of I131." Case Reports in Endocrinology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/423563.

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We herein describe a case of Marine-Lenhart syndrome with a negative TSH receptor antibody titer. A 75-year-old female presented to our hospital with malaise, palpitations, and mild fine tremors. She did not have any signs suggestive of Graves’ ophthalmopathy, including conjunctival injection, periorbital edema, or proptosis. Her laboratory data were negative for thyroid autoantibodies, including anti-thyroid peroxidase antibodies, anti-thyroglobulin antibodies, and anti-TSH receptor antibodies (TRAb). Ultrasonography of the thyroid gland revealed a tumor in the right lobe. The remaining thyro

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