Interaction of Thyroid-Stimulating Antibody with Graves’ Thyroid-Stimulating Hormone-Binding Antibody

Abstract

Objective: Evidence of anti-thyroid-stimulating hormone (TSH) antibody in Graves’ serum has been reported. We found that extremely high Graves’ anti-TSH antibodies neutralized other Graves’ thyroid-stimulating antibody (TSAb) activity. Method: TSAb-IgG was affinity-purified by Sepharose-bound Graves’ anti-TSH antibody (extremely high). Result: The thyroid-stimulating activity in affinity-purified TSAb-IgG increased about 4–5 times compared to that before purification. TSH-binding inhibitory immunoglobulin (TBII) activity in affinity-purified TSAb-IgG also increased using TSH receptor-coated tube assay. A similar increase of thyroid-stimulating activity accompanied with TBII activity was also observed in affinity-purified TSAb-IgG-F(ab′)₂. Conclusion: This suggests the possibility that either TSAb may be an anti-idiotypic antibody against anti-TSH antibody or anti-TSH antibody may be an anti-idiotypic antibody against anti-TSH receptor antibody.

Premature twins of a mother with Graves' disease with discordant thyroid function: a case report

“…Neutralization of TSI by TBII has been reported. 11 Another concept is a novel mechanism of transient hypothyroidism, recognized by Matsuura et al 12,13 in 1988. Fetal hyperthyroidism (from transplacental passage of T4) in utero owing to poorly controlled or undiagnosed maternal Graves' disease causes suppression of the neonatal pituitary-thyroid axis, with low TSH and total T4 values.…”

HLA-DPB1*0202 Is Associated with a Predictor of Good Prognosis of Graves’ Disease in the Japanese

“…Autoantibodies have been demonstrated to mimic thyrotropin and bind to the thyrotropinbinding domain of the TSHR molecule and induce a conformational change resulting in heteromeric G-proteindependent activation of adenylate cyclase [22,23]. Accordingly, in the most cases, the titers of autoantibodies against TSHR, which are assayed by two different methods, namely TBII and TSAb, the former representing the binding of antibody to TSHR and the latter the activity of adenylate cyclase, are parallel [9,24]. As mentioned earlier, about 5-10% of patient with GD are below the cut-off value for TBII at the onset [10].…”