Normal Immunoregulation of in Vitro Antibody Secretion in Autoimmune Thyroid Disease*

Abstract

Defective suppressor cell function may be a causative factor in autoimmune disease in animals and man. In autoimmune thyroid disease, decreased suppressor cell activity could, under appropriate conditions, account for excess production of thyroid autoantibodies. We evaluated suppressor cell function in patients with Graves' disease and Hashimoto's thyroiditis and in normal controls. The method used is based on the principle that immunoglobulin synthesis by pokeweed mitogen (PWM)-stimulated lymphocytes is inhibited by Concanavalin A (Con A) stimulation of suppressor T cells. We studied suppressor cell control of polyclonal immunoglobulin G (IgG) and the thyroid-specific autoantibody, antimicrosomal antibody. PWM-stimulated IgG secretion (mean ± SD) by lymphocytes from patients with Graves' disease (2797 ± 718 ng/ml) and Hashimoto's thyroiditis (2201 ± 423 ng/ml) did not differ from normal subjects (2431 ± 485 ng/ml). The addition of Con A to PWM-stimulated lymphocytes suppressed IgG production in all three groups: Graves', 475 ± 137 ng/ml; Hashimoto's, 507 ± 74 ng/ml; and normal subjects, 460 ± 156 ng/ml. The degree of suppression by the disease groups did not differ from the normal controls. Antimicrosomal antibody was detected in the concentrated, PWM-stimulated culture media of two of four Hashi-moto's lymphocytes, three of five Graves' lymphocytes, and none of nine normal controls. Con A induced marked suppression of this organ-specific antibody in all cases. We conclude that Con A-stimulated lymphocytes from patients with Hashimoto's thyroiditis and Graves' disease can suppress antimicrosomal antibody and polyclonal IgG synthesis. These findings do not support the postulate of a generalized defect of suppressor cell function in these thyroid disorders.