Anti-idiotype antibodies (Anti-Id Ab) are believed to normally exert a form of feedback control on Ab production. An abnormality in this network might lead to excess Ab production. To detect the abnormalities in immunoregulation in autoimmune
thyroid disease, we tried to demonstrate anti-Id Ab to
anti-thyroglobulin antibody (ATA) and to correlate them to the
clinical course of disease. We developed two assays, one based on the binding of anti-Id Ab to ATA (Id) and a second on the inhibitory activity of anti-Id Ab in the reaction of human
thyroglobulin (hTG) and ATA. We could not demonstrate anti-Id Ab in either assay. Possibly anti-Id Ab to ATA is not formed sufficiently to be detected in our assays, or is only present in specific phases of the course of autoimmune
thyroid disease. During studies of anti-Id Ab we found "
pepsin site" Ab in patients and normal subjects. We developed a new solid phase radioimmune assay for this Ab, an antibody which reacts with
antigens exposed on
IgG when F(ab')2 fragments of
IgG are prepared. The incidence of this Ab did not differ between patients and normal subjects.
IgG from patients with autoimmune
thyroid disease which contained high levels of anti-
pepsin site Ab, did not show any specificity for ATA (Id), nor did it inhibit the reaction between hTG (Ag) and ATA (Id). The importance of this anti-F(ab')2 antibody remains to be determined, but it does not represent an anti-Id Ab.