Detection and Properties of TSH-Binding Inhibitor Immunoglobulins in Patients with Graves’ Disease and Hashimoto’s Thyroiditis*

Endo, Keigo; Kasagi, Kanji; Konishi, Junji; Ikekubo, Katsuji; Okuno, Tatsuyo; Takeda, Yosuke; Mori, Toru; Torizuka, K

doi:10.1210/jcem-46-5-734

Cited by 292 publications

(111 citation statements)

References 21 publications

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“…In 1965, this substance called long-acting thyroid stimulator was characterized as being an antibody against a thyroid component (5). In 1978, this thyroid component was identified as the TSH receptor (RTSH) (6).…”

Section: Introductionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Role of emotional stress in the pathophysiology of Graves' disease

Falgarone¹,

Heshmati²,

Cohen³

et al. 2013

European Journal of Endocrinology

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The role of stress in the pathophysiology of Graves' disease is suggested by several clinical observations, by recent advances in immunology and by better understanding of autoimmune diseases which provides new insights into potential effects of stress hormones on T helper cell imbalance involved in the pathogenesis of autoimmune diseases. Stress management should therefore be an important part of the treatment of Graves' disease, as stress reduction may improve the effect of therapy. However, this field still requires interventional data to support stress management in the treatment of Graves' disease. European Journal of Endocrinology 168 R13-R18

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Section: Introductionmentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Role of emotional stress in the pathophysiology of Graves' disease

Falgarone¹,

Heshmati²,

Cohen³

et al. 2013

European Journal of Endocrinology

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“…GD patients without and with ophthalmopathy were 111 and 88, respectively. For anti-TSH receptor antibodies, TBII (TSH binding inhibitor immunoglobulin) activity (Rees Smith et al 1988;Endo et al 1978) was measured, because TBII activity was most frequently measured at the onset of GD as an anti-TSH receptor antibody. GD patients with potent ( ‡50%) and weak (<50%) TBII were 64 and 90, respectively.…”

Section: Clinical Manifestations Of Graves' Patientsmentioning

confidence: 99%

Association study of autoimmune thyroid disease at 5q23-q33 in Japanese patients

et al. 2003

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As part of a genome scan to locate familial Graves' disease (GD) and Hashimoto's thyroiditis (HT) genes, an autoimmune thyroid disease (AITD) susceptibility locus has recently been identified at 5q31-q33 in a Japanese population. We performed an association study using six microsatellite markers located at this locus in a set of 440 unrelated Japanese AITD patients and 218 Japanese controls. We found significant allelic association between AITD and three markers located in 5q23-q33. GD demonstrated significant associations with two of these markers, while HT did not show significant associations with any markers. Further, when patients with GD were stratified according to clinical manifestations, the association was significantly different from the other subgroup of each category. These findings suggest the presence of susceptible genes of AITD, especially distinct subgroups of GD, in or near 5q23-q33.

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“…TSAb, after the interaction with the receptor, increase cAMP accumulation causing goiter and hyperthyroidism (2,3). In atrophic thyroiditis (AT), thyroid-stimulating blocking antibodies (TSHBAb) are TSH antagonists, inhibiting TSH binding or TSH-increased cAMP levels causing thyroid atrophy and hypothyroidism (2,(4)(5)(6). The different activities of TSAb and TSHBAb suggest they might interact with different epitopes on the TSHr (2).…”

Section: Introductionmentioning

confidence: 99%

TSH receptor antibodies do not alter the function of gonadotropin receptors stably expressed in eukaryotic cells

Tonacchera

Ferrarini

Dimida

et al. 2004

European Journal of Endocrinology

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Objective: TSH receptor (TSHr) mediates the activating action of TSH on the thyroid gland resulting in the growth and proliferation of thyrocytes and thyroid hormone production. TSHr is a major autoantigen in Graves' disease (GD) and is the target for TSHr antibodies. In GD, thyroid-stimulating antibodies (TSAb) are competitive agonists of TSH. In atrophic thyroiditis (AT), thyroid-stimulating blocking antibodies (TSHBAb) are TSH antagonists. The TSHr together with the LH receptor (LHr) and FSH receptor (FSHr) are G-protein-coupled receptors with considerable amino acid homologies in the extracellular domain. We studied the cross-reactivity of the antibodies measured in sera from patients with GD or AT on the LHr and FSHr function. Methods: We tested the activity of TSAb and TSHBAb in cell lines expressing the LHr and the FSHr. To this purpose a pSVL-FSHr construct was transfected in CHO cells and one clone was used. Results: Twenty-eight sera from patients with GD and four from patients with AT, known to contain TSHr antibodies measured with a radioreceptor assay, were selected. TSAb and TSHBAb activities were measured in CHO cells expressing the TSHr (CHO-TSHr). TSAb and TSHBAb were then tested with the cell lines expressing the LHr and the FSHr for their ability to elicit cAMP accumulation or inhibit FSH/LH-induced cAMP production. None of the TSAb identified was able to stimulate cAMP increase in CHO-LHr or CHO-FSHr. Similarly, none of the TSHBAb was able to block the cAMP response induced by FSH or LH in the respective cell lines. Conclusions: Our results confirm the notion of the organ-specific nature of the TSHr antibodies.

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Detection and Properties of TSH-Binding Inhibitor Immunoglobulins in Patients with Graves’ Disease and Hashimoto’s Thyroiditis*

Cited by 292 publications

References 21 publications

MECHANISMS IN ENDOCRINOLOGY: Role of emotional stress in the pathophysiology of Graves' disease

MECHANISMS IN ENDOCRINOLOGY: Role of emotional stress in the pathophysiology of Graves' disease

Association study of autoimmune thyroid disease at 5q23-q33 in Japanese patients

TSH receptor antibodies do not alter the function of gonadotropin receptors stably expressed in eukaryotic cells

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