Correlation of microsomal antibodies with the intensity of the intrathyroidal autoimmune process in Graves' disease.
Graves' disease is an organ-specific autoimmune disease, and intrathyroidal lymphocytes seem to be the major source of thyroid autoantibodies. Consequently, the intensity of the intrathyroidal lymphocytic infiltration is generally believed to reflect the activity of the autoimmune process. We, therefore, investigated the correlation of microsomal (enzyme immunoassay), thyroglobulin (RIA), and TSH receptor antibodies (RRA) with the degree of intrathyroidal infiltration by immunoglobulin G-producing plasma cells, activated T-cells, antigen-presenting cells, and the total number of lymphocytes. The immunocompetent cells were identified immunohistologically with monoclonal antibodies for immunoglobulins kappa and lambda, UCHL1, and the S100 antibody, respectively, in 26 thyroid glands of patients suffering from Graves' disease. The intensity of lymphocytic infiltration was determined by the point-counting method and by counting all lymphocytes and the labeled lymphocytes in 3 x 51 visual fields or 3 slides/thyroid gland. Microsomal antibodies correlated significantly (P = 0.001) with the total number of lymphocytes (r = 0.86), kappa (r = 0.71), lambda (r = 0.71), UCHL1 (r = 0.9), and S100 (r = 0.9) positive cells. These correlations were also significant for thyroglobulin antibodies. However, TSH receptor antibodies showed no significant correlations with any of the populations of immunocompetent cells. Patients with preoperatively undetectable TSH receptor or microsomal antibodies showed a broad variation of intrathyroidal infiltration by the immunocompetent cells investigated. Microsomal antibody titers, therefore, seem to reflect the intensity of the intrathyroidal autoimmune process in Graves' disease better than TSH receptor antibodies. However, the broad baseline variation in intrathyroidal infiltration observed with nondetectable thyroid antibodies will not always allow determination of the intensity of the intrathyroidal autoimmune process from microsomal or thyroglobulin antibody titers.
Paschke
R
R
Service de Génétique Médicale, Faculté de Médecine, Université Libre de Bruxelles, Belgium.
Vogg
M
M
Swillens
S
S
Usadel
K H
KH
D000328:Adult; D000938:Antigen-Presenting Cells / Q000276:immunology; D001323:Autoantibodies / Q000096:biosynthesis*; D001327:Autoimmune Diseases / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D002231:Carbimazole / Q000627:therapeutic use; D006111:Graves Disease / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007145:Immunoglobulin kappa-Chains / Q000096:biosynthesis; D007146:Immunoglobulin lambda-Chains / Q000096:biosynthesis; D008214:Lymphocytes / Q000276:immunology; D008861:Microsomes / Q000276:immunology*; D010950:Plasma Cells / Q000276:immunology; D011441:Propylthiouracil / Q000627:therapeutic use; D011989:Receptors, Thyrotropin / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013954:Thyroglobulin / Q000037:antagonists & inhibitors; D013961:Thyroid Gland / Q000276:immunology*; D013972:Thyrotropin / Q000096:biosynthesis
D001323:Autoantibodies; D007145:Immunoglobulin kappa-Chains; D007146:Immunoglobulin lambda-Chains; D011989:Receptors, Thyrotropin; C006606:anti-thyroglobulin; D011441:Propylthiouracil; D002231:Carbimazole; D013972:Thyrotropin; D013954:Thyroglobulin