[On the mechanisms of thyrocyte proliferation and death in autoimmune thyroid diseases].

Lymphocytes isolated from diffuse toxic goiter (Graves' disease, GD) stimulate the proliferation of "normal" thyrocytes (isolated from euthyroid goiter) in primary culture, and give them the properties of GD-thyrocytes (loss of sensitivity to the growth-promoting factors of FCS and lesser capacity of binding antibodies from GD patients' serum). The complement-free sera of GD patients (but not the sera of patients with Hashimoto's thyroiditis, HT) induce the death of "normal" thyrocytes more rarely than full-complement sera do. Both types of serum cytotoxicity are manifested on GD-thyrocytes much more rarely than on "normal" cells.

Increase in serum concentration of FAS ligand as a possible mechanism for antithyroid cytotoxicity during autoimmune thyroid diseases.

We studied the dependence of serum cytotoxic activity on the contents of soluble apoptosis receptor and its soluble ligand in patients with autoimmune thyroid diseases.

[Blood serum immunoglobulins from patients with juvenile struma reduce the cAMP level in isolated human thyrocytes].

Clinico-hormonal examinations of 19 patients with juvenile struma revealed in many of them signs of latent hypothyrosis (increased age-specific level of blood serum TTH level and hyperergic reaction to TRH). Incubation of thyrocytes isolated from perinodular tissue of patients with euthyroid nodular goiter with IgG isolated from the blood serum of patients with juvenile struma resulted in a reliably lower content of cAMP in the cells than after thyrocyte incubation with IgG isolated from the blood serum of 9 healthy donors. This is indicative of the presence of thyroblocking antibodies in the blood serum of patients with juvenile struma.

[Interactions between serum antibodies of patients with autoimmune thyropathies and isolated cells of diffuse toxic euthyroid nodular goiter].

Blood sera of 46 patients with diffuse toxic goiter (DTG) and of 48 ones with Hashimoto's thyroiditis (HT) were tested for antibodies--complement-mediated cytotoxicity carriers (ACMMC). ACMCC targets were isolated DTG cells and cells of euthyroid nodular goiter (ENG) perinodular tissue. Antimicrosomal antibodies were assayed in the sera by indirect immunofluorescence and antibodies to all thyrocyte surface antigens isolated from both tissue samples were determined by solid-phase enzyme immunoassay.

[Determination of autoantibodies to thyrotropin receptors in patients with diffuse toxic goiter].

The blood level of antithyroid autoantibodies to TSH receptors was determined in patients with toxic goiter (TG) before and during antithyroid therapy using two biological methods (by the increment in the cAMP level in slices and primary monolayer culture of human thyroid cells) and a radioreceptor method (by inhibition of TSH binding with its receptors from the animal thyroid). Comparison of the results of these three methods has shown that all methods are almost equally valuable for diagnosis of new cases of TG. However the biological method was shown to be more sensitive and informative with regard to predicting the time of immunological remission during antithyroid therapy.