Thyroid-stimulating hormone inhibits Fas antigen-mediated apoptosis of human thyrocytes in vitro

Kawakami, Ayako

doi:10.1210/en.137.8.3163

Cited by 40 publications

(34 citation statements)

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“…Fas antigen is functionally expressed on the surface of thyrocytes, and TSH inhibits Fas antigen-mediated apoptosis of thyrocytes resulting in the promotion of growth of the thyroid gland [15]. Intercellular adhesion molecule-1 and class II MHC have been implicated as contributing factors for numerous diseases, including autoimmune thyroid diseases, and TSH could downregulate their interferon-γ-mediated expression [16,17,18,19].…”

Section: Discussionmentioning

confidence: 99%

Coexistence of Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma and Graves' Hyperthyroidism

et al. 2013

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Background: Coexistence of thyroid-stimulating hormone (TSH)-secreting pituitary adenoma (TSHoma) with Graves' disease has been rarely reported. We describe a female patient displaying TSHoma with Graves' disease and who presented initially with inappropriate TSH values. Case Report: A 36-year-old woman presented with signs of thyrotoxicosis, small and vascular goiter and mild bilateral exophthalmos. Thyroid function tests showed hyperthyroxinemia and normal TSH values despite the use of different assays. Heterophile antibody testing result was negative. The patient underwent total right lobectomy with partial left lobectomy after 18 months of carbimazole treatment. Histology confirmed Graves' disease. Symptoms of thyrotoxicosis recurred 2 months later. Thyroid function tests showed hyperthyroxinemia and elevated TSH values. Investigations were consistent with a 10-mm TSHoma. The patient underwent a trans-sphenoidal tumor resection following preoperative lanreotide preparation. Histological examination and immunocytochemistry concluded to a pure TSH-producing tumor. There was no evidence of tumor recurrence after 18 years of follow-up. Conclusion: Association of TSHoma with Graves' disease should be carefully taken into account, especially when TSH values are not compatible with either the clinical history or other thyroid functions tests.

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Section: Discussionmentioning

confidence: 99%

Coexistence of Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma and Graves' Hyperthyroidism

et al. 2013

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“…In normal circumstances, the Fas pathway is inhibited, whereas in inflammation, it is activated by cytokines [153]. In vitro studies have shown that TSH inhibited Fas-mediated apoptosis, while the absence of TSH induced apoptosis [154]. A combination of IFN-γ with TNF-α or IL-1β stimulated the Fas-activated apoptosis in cultured thyroid follicular cells [155].…”

Section: Thyroid Destructionmentioning

confidence: 99%

Hashimotos Thyroiditis: From Genes to the Disease

Zaletel¹,

Gaberšček

2011

171

168

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Hashimoto’s thyroiditis (HT) is the most prevalent autoimmune thyroid disorder. Intrathyroidal lymphocytic infiltration is followed by a gradual destruction of the thyroid gland which may lead to subclinical or overt hypothyroidism. Biochemical markers of the disease are thyroid peroxidase and/or thyroglobulin autoantibodies in the serum which are present with a higher prevalence in females than in males and increase with age. Although exact mechanisms of aetiology and pathogenesis of the disorder are not completely understood, a strong genetic susceptibility to the disease has been confirmed predominantly by family and twin studies. Several genes were shown to be associated with the disease occurrence, progression, and severity. Genes for human leukocyte antigen, cytotoxic T lymphocyte antigen-4, protein tyrosine phosphatase nonreceptor-type 22, thyroglobulin, vitamin D receptor, and cytokines are considered to be of utmost importance. Amongst endogenous factors for the disease development, the attention is focused predominantly on female sex, pregnancy with postpartum period and fetal microchimerism. Environmental factors influencing HT development are iodine intake, drugs, infections and different chemicals. Disturbed self-tolerance accompanied by the increased antigen presentation is a prerequisite for the HT occurrence, whereas proper interaction of thyroid cells, antigen presenting cells, and T cells are necessary for the initiation of thyroid autoimmunity. Secreted cytokines lead predominantly to T-helper type 1 (Th1) response as well as to Th 17 response which has only recently been implicated. Final outcome of HT is thyroid destruction which is mostly a consequence of the apoptotic processes combined with T-cell mediated cytotoxicity.

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“…The decrease in the number of Treg cells (especially CD25+) induced development of lymphocytic infiltrations in the thyroid and hypothyroidism [11]. Thyroid dysfunction is connected with thyrocyte apoptosis in the vicinity of active lymphocytes [12,13,14,15]. Numerous fibroblasts and collagen fibres may be observed in the thyroid tissue in Hashimoto’s thyroiditis.…”

Section: Introductionmentioning

confidence: 99%

Interactions of Lymphocytes, Thyrocytes and Fibroblasts in Hashimoto’s Thyroiditis: An Immunohistochemical and Ultrastructural Study

Beń‐Skowronek¹,

Szewczyk²,

Ciechanek³

et al. 2011

Horm Res Paediatr

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Background: The mechanism of autoimmune reaction, a diffuse process consisting of a combination of epithelial cell destruction, lymphoid cellular infiltration, and fibrosis in Hashimoto’s thyroiditis, is not well known. The aim of this study was to analyse the cell subsets in thyroid tissue of patients with Hashimoto’s thyroiditis. Methods: We studied paraffin-embedded thyroid specimens obtained from children with Hashimoto’s thyroiditis and children without an autoimmune thyroid disease. Mononuclear T cells were detected by means of CD3+, CD4+, CD8+ antibodies, B cells by CD79 alpha+ antibodies, and antigen-presenting cells by CD1a+ antibodies, and they were counted in every 1,000 cells. The specimens from each patient were routinely estimated and investigated under the electron microscope. Results: In Hashimoto’s thyroiditis, we observed a statistically significant increase in T suppressor/cytotoxic cells CD8+ (20.54 ± 0.68%) in comparison to the control group (0.65 ± 0.30%), simple goitre (4.01 ± 5.54%) and nodular goitre (8.53 ± 2.37%), and a statistically significant increase in plasma CD79 alpha+ cells (31.65 ± 9.11%) in comparison to the control group (4.11 ± 1.94%), simple goitre (1.83 ± 0.64%) and nodular goitre (5.22 ± 1.63%). Simultaneously, we observed a low number of CD4+ T helper cells in the thyroid gland (0.93 ± 0.99%) in Hashimoto’s thyroiditis (0.19 ± 0.05% in the control group, 1.05 ± 2.71% in simple goitre, 2.03 ± 1.06% in nodular goitre). The ultrastructural investigations showed interactions between T cells, plasmocytes, fibrocytes and thyrocytes leading to apoptosis of thyrocytes. An immunological synapse between T cells, plasmocytes and thyrocytes in the thyroid gland was noticed. Conclusions: In Hashimoto’s thyroiditis, autoantigen presentation in combination with a low number of CD4+ T helper cells and a high number of CD8+ cells and plasmocytes caused the development of a cytotoxic reaction against thyrocytes, leading to apoptosis of the thyrocytes.

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Thyroid-stimulating hormone inhibits Fas antigen-mediated apoptosis of human thyrocytes in vitro

Cited by 40 publications

References 0 publications

Coexistence of Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma and Graves' Hyperthyroidism

Coexistence of Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma and Graves' Hyperthyroidism

Hashimotos Thyroiditis: From Genes to the Disease

Interactions of Lymphocytes, Thyrocytes and Fibroblasts in Hashimoto’s Thyroiditis: An Immunohistochemical and Ultrastructural Study

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