Peripheral blood lymphocytes from normal individuals can be induced to secrete immunoglobulin G antibodies against self-antigen thyroglobulin in vitro.

Autoantibodies to the self-antigen thyroglobulin (Tg) are usually not found in sera of normal individuals, but are often present in sera of patients with autoimmune thyroid diseases. To determine if the presence of such autoantibodies could be due to the abnormal appearance of self-reactive B cells, which are otherwise absent in normal subjects, or to an alteration in the mechanisms regulating such B cells, peripheral blood lymphocytes (PBL) from normal individuals and patients with autoimmune thyroid diseases were cultured and stimulated in vitro with the polyclonal stimulant pokeweed mitogen (PWM). A modified plaque assay was used to enumerate cells secreting protein A-binding immunoglobulins (Igs) and specific antibodies against Tg. PBL from all individuals tested, including normal subjects (n = 26), could be induced by PWM to produce antibodies against Tg in vitro and these antibodies were of IgG isotypes. PBL from patients with detectable serum anti-Tg had more inducible cells secreting anti-Tg [27,000 +/- 10,700 (+/- SD)/10(6) PBL] than those from patients with autoimmune thyroid diseases, who had no detectable serum anti-Tg (8,000 +/- 5,000), and those from normal individuals (7,200 +/- 4,200). The demonstration of inducible mature (IgG) anti-Tg-producing cells in normal individuals suggests that subclinical autoimmunity against certain self-antigens may be a normal phenomenon in man and that its escalation into clinical autoimmune conditions is prevented through regulation of the specific self-reactive cells.