title: [Changes of peripheral mononuclear cell subpopulations in autoimmune thyroid diseases].
abstract: To estimate abnormalities in humoral or cellular immunity that relate to the etiologies of Graves' disease (GD) and Hashimoto's thyroiditis (HT), peripheral mononuclear cell subpopulations were enumerated by an immunofluorescence technique using monoclonal antibodies. Also antithyrotropin receptor antibodies (thyrotropin-binding inhibitor immunoglobulin, TBII) were measured by the radioreceptor assay according to Smith's method; and antithyroglobulin antibodies (TGHA) and antithyroid microsomal antibodies (MCHA), by the tanned red cell hemagglutination technique. The data obtained were analyzed for the count of peripheral total white cells, lymphocytes and granulocytes, and to the level of serum free thyroxine (T4), free T4 index (FT4I) and free triiodothyronine index (FT3I). Peripheral white cells tended to be decreased in some cases of GD and HT. The absolute count of lymphocytes was slightly increased in GD but did not change in HT. On granulocytes (neutrophils mainly), the absolute count was considerably decreased in hyperthyroid GD. In this disease, FT3I showed significantly positive correlations to the percentage and absolute count of peripheral lymphocytes, whereas FT4I revealed significantly negative correlations to the percentage and count of granulocytes. These facts indicate that lymphocytosis and granulocytopenia in GD might be ascribed partially to the direct effects of thyroid hormones. The percentage of peripheral OKT3-positive cells (common T lymphocytes) was significantly decreased in untreated cases of GD, showing negative correlations to FT4, FT4I and FT3I. The absolute count of OKT4-positive cells (inducer/helper T lymphocytes) was increased in untreated cases of GD and hyperthyroid and euthyroid cases receiving antithyroid drugs (ATD) for GD. But peripheral OKT8-positive cells (suppressor/killer T lymphocytes) was significantly decreased in HT. The percentage of peripheral OKT8-positive cells in GD was also decreased in untreated and remitted cases, but slightly more increased in ATD-medicated cases than in nonmedicated cases. The ratios of OKT4-positive cells to OKT8-positive cells (OKT4+/OKT8+ ratios) were significantly increased in untreated, ATD-medicated euthyroid and remitted cases of GD, and in HT. It seems that ATD may exert direct effects on OKT8-positive cells.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000974:Antibodies, Antinuclear / Q000032:analysis; D000911:Antibodies, Monoclonal / Q000032:analysis; D001327:Autoimmune Diseases / Q000276:immunology*; D006111:Graves Disease / Q000276:immunology; D006801:Humans; D006980:Hyperthyroidism / Q000276:immunology; D007037:Hypothyroidism / Q000276:immunology; D008214:Lymphocytes / Q000145:classification*; D011956:Receptors, Cell Surface / Q000276:immunology; D011989:Receptors, Thyrotropin; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D013959:Thyroid Diseases / Q000276:immunology*; D013967:Thyroiditis, Autoimmune / Q000276:immunology
chemical_list: D000974:Antibodies, Antinuclear; D000911:Antibodies, Monoclonal; D011956:Receptors, Cell Surface; D011989:Receptors, Thyrotropin