Cellular and antibody mediated cytotoxicity in autoimmune thyroid disease

Publisher Website
Google Scholar
Abstract
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 cytoxicity (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. In conclusion, we demonstrated increased ADCC and NK cell activity in Hashimoto's thyroiditis but normal NK cell activity in euthyroid Graves' disease. Like in HT, ADCC is associated with titres of Mab in sera of Graves' disease patients but was also detectable in Mab-negative sera, which led us to suggest that a hitherto unknown cytotoxic antibody exists which is not measurable by passive haemagglutination for Mab.

This publication has 0 references indexed in Scilit: