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Biomedical subjects

E P Artemova

Publications and source records attributed to E P Artemova.

17 recordsLinked to original sources
PubMed1992

[Role of immune complexes in thyroid diseases].

To elucidate the immune complex (thyroglobulin-antibody, Tg-Ab) role in thyroid hormone formation, in vitro iodination of Tg--AB immune complex, bovine intact Tg and that of the patient with euthyroid goiter and partially purified AB to Tg were studied. We compared the amount of iodamine acids (MIT, DIT, T4/mole of Tg) forming during iodination in immune complex with other samples. The results suggest that Tg being in complex with antibodies (up to 30-40 mole of antibodies/mole of Tg) is iodinated forming the enough amount of MIT, decreased amount of DIT and T4. A MIT fraction increase is connected with additional iodination of complex antibodies. We suggest that such processes may take place in the patient body and be involved in pathogenesis of thyroid disease.

Animals↗
PubMed1990

[Activation of immunity in patients with recurrent goiter].

The authors studied the morphological pattern of the thyroid gland in patients with goiter and in those with a recurrence of the disease. They found lymphoid infiltration and autoimmune thyroiditis twice more frequently in patients with recurrent goiter. Dynamic study of features of the immune and thyroid status of patients with recurrent goiter after the operation led to the isolation of a group of patients with an increase in the relative content of T and B lymphocytes and thyroxine. These changes preceded the recurrence of goiter.

Autoantibodies↗
PubMed1981

[Effect of anti-thyroid antibodies on thyroid hormone secretion].

Secretory thyroid function was studied in animals with experimental autoimmune thyroiditis and in rats with passive immunization by antithyroid antibodies. The lowering of colloid endocytosis and thyroglobulin proteolysis accompanied by complete suppression of total thyroxin secretion stimulation was shown to occur in autoimmune thyroiditis. Injection to the rats of antibodies in the form of IgG gamma 2 fraction led to the reduced colloid output from the follicles, diminished secretion of triiodothyronine and to a pronounced suppression of thyroxin secretion stimulation. It is concluded that the lowering of colloid endocytosis and proteolytic enzymes is caused by insufficient production of TSH. Antithyroid antibodies should be treated as responsible for suppressed thyroxin secretion into the blood.

Animals↗
PubMed1976

[Congenital disorders of the thyroid gland in experimental litters obtained from mothers subjected to immunization and the action of I-131].

I131 injected to rabbits immunized with homologous thyroid gland on the 19th-20th day of pregnancy led to congenital disturbances of the thyroid gland in the experimental litters in the I and II generations. The functional activity and the activity of proteolytic enzymes of the thyroid gland decreased by the 30th day of the postnatal development. There was revealed a distinct correlation between the content in the thyroid gland of the experimental litters of DIT + MIT and of organic forms--T3 + T4. During the first days after birth DIT + MIT content showed a sharp fall and increased by the 30th day; on the contrary, iodine binding into organic forms decreased with the progress of age. Histological examination of the thyroid glands in the experimental litters demonstrated lymphoid-plasmocytic infiltration, along with connective tissue proliferation, which led to a marked sclerosis and fibrosis of tissues, hypofunction. Beginning from the age of one month there was seen an extensive nodular proliferation, which possibly served as the beginning of parenchymatous goiter formation. The appearance of lymphoid-plasmocytic infiltration in the thyroid gland of the II generation is considered to be the result of congenital predisposition to the autoimmune thyroiditis inlaid in the memory cells and intensified during birth.

Amino Acids↗
PubMedDate not supplied

[Suppression of development of autoimmune thyroiditis during prolonged stimulation of T-cellular immunity].

The purpose of this experiment was to investigate the suppression of autoimmune thyroiditis in guinea-pigs by prolonged stimulation of T-cellular immunity with T-activin, a thymic hormone. The development of experimental autoimmune thyroiditis (EAT) at early stages was shown to be characterized by deficiency of T-cells of helper and suppressor phenotypes, hypersecretion of thyroid hormones and insignificant development of a thyroid autoimmune process. With disease development indices of peripheral blood immunity of guinea-pigs were close to normal, and the frequency and degree of lymphoid infiltration of the gland were increased in parallel with the development of hypofunction of the organ. Immuno-correction of developing EAT with injections of T-activin according to our scheme resulted in a prolonged stimulation of T-cellular immunity, prevented sensitization of lymphocytes with thyroid antigens, increased secretion of the thymic hormones in parallel with a decrease in a degree of lymphoid-plasmacytic infiltration from thyroid tissues, indicating suppression of the disease.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Partial blocking of the organofaction of iodine with thyroglobulin antibodies].

The influence is studied of purified thyroglobulin antibodies on a stage of thyroid hormone formation, i.e. iodine organofication, using a method of inorganic iodine replacement by potassium perchlorate. A decreased marker uptake by the thyroid and a delay of iodide inclusion into organic components were observed after incubation of rat thyroid slices and injection of a similar antiserum to normal rats 24 hours before radioactive iodine administration. The data obtained indicate that the disturbance of iodine organofication is possible under thyroglobulin antibody effect, accompanied by the thyroid autoimmune process development.

Animals↗
PubMedDate not supplied

[ T- and B-lymphocyte populations in thyroid pathology].

Examination of cellular and humoral immunity in patients with thyroid pathology demonstrated that autoimmune forms were attended by T cell deficiency with an excess of B cells and circulating antithyroid autoantibodies. The blood content of T and B lymphocytes was within the normal range in patients with nontoxic goiter, but circulating autoantibodies to the thyroid gland were found in 40% of cases. Examination of the blood in patients with diffuse toxic goiter of moderate severity at the early periods after a course of chemotherapy showed no normalization of the cellular and humoral immunity indices.

Antibody Formation↗
PubMedDate not supplied

[Effect of passive lymphocyte transfer on the course of autoimmune thyroiditis in guinea pigs].

Effects of adoptive transfer of T lymphocytes from normal animals (intact and in vitro pretreated with tactivin) on the expression of experimental autoimmune thyroiditis in guinea pigs were studied. Thyroiditis development was characterized by immunocompetent cell imbalance, formation of antithyroid antibodies, development of diffuse and focal lymphoid-plasmacytic infiltration in thyroid tissues. A single injection of intact T lymphocytes normalized the immunity status and significantly (by three times) reduced the lymphoid infiltration area but did not augment thyroxin secretion in animals with thyroiditis. Immunotherapy of the condition with tactivin-activated lymphocytes was found more effective, for it enhanced serum thyroxin secretion, normalized the immunity status, and reduced lymphoid-plasmacytic infiltration of the thyroid.

Animals↗
PubMedDate not supplied

[The effect of thyrotropic hormone on processes mediating the cytotoxicity of antithyroid antibodies].

Administration of 3 units of thyrotropic hormone to rabbits with autoimmune thyroiditis and hypothyroidism led to reduction of the I131 absorption by the thyroid gland and to increase in the activity of proteolytic enzymes of the gland. Apparently, in autoimmune thyroiditis disturbances at the stages of the iodide incorporation into the gland were irreversible; proteolysis depression was apparently secondary. Possibly the mentioned disturbances were associated with the circulating antithyroid antibodies.

Animals↗