[Immunological aspects of auto-immune thyroid diseases (author's transl)].
Sufficient evidence exists to relate auto-immune thyroid diseases (including both Graves-Basedow's disease and Hashimoto's thyroiditis) to primary disturbances of the lymphatic system. Currently available data underline the importance of immunological factors, either humoral or tissular, in the physiopathological expression of these diseases, their basic genetic disorder appearing to be a specific lack of "suppressor" T lymphocytes. This results in the survival and multiplication of an unwanted clone, appearing by chance, of "helper" T lymphocytes directed specifically towards the thyroid. These lymphocytes then cooperate with groups of previously existing appropriate B lymphocytes, which then produce immunoglobulins directed against the thyroid. Subtle genetic differences determine the appearance of either Graves-Basedow's disease or Hashimoto's thyroiditis with their typical clinical manifestations. In fact, these subtle genetic differences between the different groups of patients with Graves-Basedow's disease may result in the total absence of immunity control (thus preventing any immunological remission) whereas partial lack may occur with the possibility of remission. The role of stress in the development of hyperthyroidism may be related to the effects of an aggression on a T lymphocyte population already partially deficient.
D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology*; D006111:Graves Disease / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D008222:Lymphokines / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000276:immunology; D013959:Thyroid Diseases / Q000235:genetics / Q000276:immunology*; D013961:Thyroid Gland / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000276:immunology
D001323:Autoantibodies; D008222:Lymphokines
Aspects immunologiques des maladies auto-immunes de la thyroïde.