Extrathyroidal synthesis and biologic action of thyroid receptor antibody (TRAb) in Graves' disease

1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S352-S354 ◽  
Author(s):  
R. Paschke ◽  
H. G. Heinze ◽  
J. Teuber ◽  
R. Schmeidl ◽  
K. H. Usadel
Keyword(s):  
Nude Mice ◽  
Radioiodine Therapy ◽  
Thyroid Tissue ◽  
Graves Disease ◽  
Receptor Antibody ◽  
Radioligand Assay ◽  
Biologic Activity ◽  
Thyroid Receptor ◽  
Bio Assay

Abstract. In a patient with Graves' disease who underwent thyroidectomy with subsequent radioiodine therapy thyroid receptor antibody could be detected by radioligand assay. No thyroid tissue could be detected by 131I-scintiscanning. Thyroglobulin was repeatedly negative. Biologic activity of this patients serum could be demonstrated in the nude mice bio assay. 131I-incorporation and secretion of human thyroglobulin could be stimulated by injecting thymusdysplastic nude mice with transplants of thyroid tissue from a patient with Graves' disease with the athyroid patients serum. These results demonstrate evidence for extrathyroidal production and biological actiivty of TRAb in vivo.

The relationship between thyroid receptor antibody and anti mullerian hormone in Graves' disease

2019 ◽  
Author(s):  
Keziban Demir ◽  
Hakan Kursat ◽  
Sevde Yazici ◽  
Hamide Pişkinpaşa ◽  
Evin Bozkir ◽  
...  
Keyword(s):  
Graves Disease ◽  
Receptor Antibody ◽  
Thyroid Receptor ◽  
The Relationship

scholarly journals Demonstration of reduced in vivo surface expression of activating mutant thyrotrophin receptors in thyroid sections

2002 ◽  
pp. 163-171 ◽  
Author(s):  
M Sequeira ◽  
B Jasani ◽  
D Fuhrer ◽  
M Wheeler ◽  
M Ludgate
Keyword(s):  
Molecular Mechanisms ◽  
Thyroid Tissue ◽  
Surface Expression ◽  
Germline Mutations ◽  
Antigen Retrieval ◽  
Graves Disease ◽  
Paraffin Sections ◽  
Gain Of Function

OBJECTIVE: Thyroid function and growth are controlled by TSH. Hyperthyroidism can be due to Graves' Disease (GD), in which thyroid-stimulating antibodies mimic TSH, or gain-of-function mutations in the TSH receptor (TSHR). These activating mutations have poor surface expression when assessed in non-thyroidal cells in vitro but nothing is known of their in vivo behaviour. Several TSHR antibodies have been produced but none has been applied to thyroid paraffin sections. This study aimed to develop a technique suitable for use on paraffin sections and apply it to investigate TSHR expression in thyroids harbouring activating TSHR germline mutations compared with normal and GD thyroids. DESIGN AND METHODS: Immunocytochemistry coupled with antigen retrieval, using a spectrum of antibodies to the TSHR, was applied to paraffin sections of GD thyroid tissue. Subsequently, TSHR immunoreactivity was examined in three normal thyroids, three patients with GD and three patients with familial hyperthyroidism, due to different gain-of-function TSHR germline mutations, using the optimised protocol. RESULTS: Two antibodies, A10 and T3-495, to the extracellular domain (ECD) and membrane spanning region (MSR) of the TSHR respectively, produced specific basolateral staining of thyroid follicular cells. In normal and GD thyroids, basolateral staining with T3-495 was generally more intense than with A10, suggesting a possible surfeit of MSR over ECD. Graves' Disease thyroids have more abundant TSHR than normal glands. In contrast, thyroids harbouring gain-of-function mutations have the lowest expression in vivo, mirroring in vitro findings. CONCLUSIONS: The development of an immunocytochemical method applicable to paraffin sections has demonstrated that different molecular mechanisms causing hyperthyroidism result in the lowest (mutation) and highest (autoimmunity) levels of receptor at the thyrocyte surface.

Evidence of in vivo iodine-induced hyperthyroidism in hyperfunctional autoimmune and autonomous human thyroid tissue xenotransplanted to nude mice

1987 ◽  
Vol 65 (4) ◽  
pp. 197-201 ◽  
Author(s):  
P. -M. Schumm-Draeger ◽  
R. Senekowitsch ◽  
F. -D. Maul ◽  
H. J. C. Wenisch ◽  
C. R. Pickardt ◽  
...  
Keyword(s):  
Nude Mice ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Human Thyroid Tissue

BEHAVIOUR OF THYROID TISSUE FROM PATIENTS WITH GRAVES' DISEASE IN NUDE MICE

1984 ◽  
Vol 59 (1) ◽  
pp. 175-177 ◽  
Author(s):  
JACQUES LECLERE ◽  
MARIE CHRISTINE BENE ◽  
ADRIEN DUPREZ ◽  
GILBERT FAURE ◽  
JEAN LOUIS THOMAS ◽  
...  
Keyword(s):  
Nude Mice ◽  
Thyroid Tissue ◽  
Graves Disease

EVALUATION OF TSH RECEPTOR ANTIBODY BY ‘NATURAL IN VIVO HUMAN ASSAY’ IN NEONATES BORN TO MOTHERS WITH GRAVES’ DISEASE

1989 ◽  
Vol 30 (5) ◽  
pp. 493-503 ◽  
Author(s):  
H. TAMAKI ◽  
N. AMINO ◽  
Y. IWATANI ◽  
J. TACHI ◽  
M. KIMURA ◽  
...  
Keyword(s):  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibody ◽  
Tsh Receptor Antibody

scholarly journals The prognostic value of thyroid-stimulating immunoglobulin in the management of Graves’ disease

2021 ◽  
Vol 12 ◽  
pp. 204201882110449
Author(s):  
Yulin Zhou ◽  
Mengxi Zhou ◽  
Yicheng Qi ◽  
Weiqing Wang ◽  
Xinxin Chen ◽  
...  
Keyword(s):  
Odds Ratio ◽  
Prognostic Value ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Inhibition Assay ◽  
Hormone Binding ◽  
Receptor Antibody ◽  
End Of Treatment ◽  
Binding Inhibition ◽  
Thyroid Receptor

Background: The bioassay of thyroid-stimulating immunoglobulin was reported to have a similar performance to the commonly used thyroid-stimulating hormone binding inhibition assay, also known as thyroid receptor antibody assay. The normal reference range of thyroid receptor antibody levels indicates the withdrawal of anti-thyroid drugs in the recent clinical guidelines. Methods: A prospective, longitudinal observational study was conducted to evaluate the prognostic value of thyroid-stimulating immunoglobulin in patients with Graves’ disease. Results: A total of 77 patients with Graves’ disease treated with anti-thyroid drugs were in a continuous follow-up until 1 year after anti-thyroid drugs discontinuation. Commercial kits of thyroid-stimulating immunoglobulin and M22-thyroid-stimulating hormone binding inhibition assay were used and compared. Thyroid-stimulating immunoglobulin was all negative in healthy controls, Hashimoto thyroiditis, and subacute thyroiditis. Thyroid-stimulating immunoglobulin value was highest in untreated patients with Graves’ disease ( p < 0.001). Under anti-thyroid drugs treatment, thyroid-stimulating immunoglobulin value decreased gradually. A total of 21 patients had positive thyroid-stimulating immunoglobulin at the end of treatment. According to clinical fate of patients with Graves’ disease after withdrawal of anti-thyroid drugs, thyroid-stimulating immunoglobulin value and positivity in patients with relapse were significantly higher than that reported in patients with remission ( p = 0.001, p < 0.001). After adjustment for age, gender, initial thyroid receptor antibody, initial thyroid-stimulating immunoglobulin, and thyroid receptor antibody at the end of treatment, the odds ratio of positive thyroid-stimulating immunoglobulin for the risk of relapse was 33.271 (95% confidence interval: 4.741–233.458, p < 0.001) and odds ratio of quantitative thyroid-stimulating immunoglobulin was 1.009 (95% confidence interval: 1.002–1.015, p < 0.001). Conclusion: Thyroid-stimulating immunoglobulin is a good predictor of relapse in patients with Graves’ disease treated with anti-thyroid drugs. It might be safer to discontinue anti-thyroid drugs when thyroid-stimulating immunoglobulin and thyroid receptor antibody were both negative.

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