Acta endocrinologica. Supplementum最新文献

Among the various autoantibody tests applied in research and clinical practice, the determination of thyroid microsomal (TMAb) and thyroglobulin antibodies (TgAb) still retains its strong value in the screening for thyroid autoimmunity. The presence in the serum of TMAb is almost invariably associated with thyroid autoimmune disease or focal thyroiditis. The appearance of TMAb together with elevated serum-TSH in subclinical autoimmune thyroiditis strongly suggests progression to overt hypothyroidism. Pregnant women with positive TMAb and/or TgAb run an increased risk for post-partum painless thyroiditis with transient thyrotoxicosis and subsequent hypothyroidism. After delivery also a relapse of previously unrecognized Graves' thyrotoxicosis may occur. Thyroid antibody determination is not a valuable tool to discriminate autoimmune thyroiditis from thyroid malignancies. TMAb and TgAb determination helps to recognize individuals with thyroid autoimmunity among patients with non-thyroid autoimmune diseases such as Addison's disease and Type I diabetes mellitus.

Thyroid cell proliferation has been studied using an in vitro system of rat thyroid follicular cell strain (FRTL-5). While growing in continuous culture, this strain is still differentiated and non-tumourigenic. Both advantages and limitations in the use of such system for studies of thyroid cell growth should be considered. Some obvious limitations should be considered, such as the species (rat) from which FRTL-5 cells were originated, their long-term growth outside the animals, the presence of a chronic TSH stimulation. On the other hand, several advantages as the growth in hormonally and chemically defined media, their dependence upon TSH in the medium, their genetic homogeneity and their widespread use in many laboratories render the FRTL-5 strain a useful experimental tool. Studies on cell proliferation and mechanism of action of hormones, growth factors and human autoimmune IgG have been and are being performed, with the assumption that FRTL-5 cells are the in vitro equivalent of thyroid follicular cells.

Antibody-dependent cell-mediated cytotoxicity (ADCC) and natural killer (NK) cell-mediated cytotoxicity was measured in patients with Hashimoto's thyroiditis (HT) and Graves' disease (GD) using a cytotoxicity assay against thyroid target cells. In the ADCC assay, mean +/- SD specific lysis produced by sera from patients with HT was 21.7 +/- 10% compared t 6.2 +/- 3.9% from normal subjects. In the NK assay, cytotoxicity was significantly increased using lymphocytes from HT patients as effector cells. At effector: target (E:T) cell ratios of 50:1 and 25:1, mean specific lysis +/- SD was 18.3 +/- 14.3% and 14 +/- 11.6%, respectively, compared to 3.7 +/- 2.1 and 3.1 +/- 2.1, respectively, for normals. In Graves' disease, 9 of 19 patients had elevated cytotoxicity, whereas no significant changes of ADCC could be found either, as determined in thyrotoxic patients, after 6 months and at the end of a one-year antithyroid drug treatment. Eight of 19 patients showed normal cytotoxicity (mean % specific lysis 2.5 +/- 3.1% compared to 2 +/- 2.9% in normal controls) and low titres of microsomal antibodies (Mab), 3 patients had significantly increased cytotoxicity (mean specific lysis 27.6 +/- 10%) in the presence of high titres of Mab, whereas 8 patients evidenced high values for cytotoxicity (mean specific lysis 24.5 +/- 14.1%) but low titres of Mab. NK cell activity, determined in euthyroid Graves' disease patients either under antithyroid drug therapy or in remission, was not significantly different than that of normal subjects at all E:T cell ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

The modulation of HLA-D expression of thyroid epithelial cells (TEC) was studied in vitro by means of immunofluorescence. Under serum-free culture conditions, TSH and TSH-receptor antibodies induce HLA-D on TECs derived from GD-patients. Serum-free culture conditions provide a higher availability of TSH-receptors by a 'right side right' polarity of the cellular morphology. There was no evidence for IFN-gamma producing cell contaminations on GD-TECs. TSH in contrast to IFN-gamma does not induce HLA-DQ on TECs. HLA-DQ is not displayed by spontaneously class-II antigen expressing GD-TECs. Methimazole as well as perchlorate do not suppress HLA-D expression of TECs.