Regulation of anti-TSH receptor antibody (anti-TSH-R antibody) in Graves' patients
(n = 11) by anti-idiotypic antibody was studied using patients sera before and after
one year of Methimazole treatment. Patients sera with high level of anti-TSH-R antibody
(110 + 41.9 U/I) were incubated with pooled control and autologous (with low level
or anti-TSH-R antibody negative) sera containing equimolar IgG G. The mixture was
centrifuged and the supernatants were tested for anti-TSH-R antibodies (TRAK, Henning).
It was found that the autologous sera from patients with remission were able to suppress
significantly the titre of anti-TSH-R antibodies (p < 0.001), whereas the controls
were capable of a less remarkable inhibition. F(ab')2 fragments of autologous IgG
from remission could also suppress the levels of TSH-R antibodies. It was concluded
that anti-anti-TSH-R antibodies in sera of Graves' patients might be, at least in
part, responsible for inducing and maintaining remission and suppression of autoantibodies
to TSH-R. It is hypothesized that the idiotype system is part of the network of natural
autoantibodies and that its perturbation may give rise to pathogenetic antibodies.
On the basis of this observation the autologous sera could have therapeutical implication
in an accelerated remission of hyperthyroidism in Graves' disease.