A COMPARATIVE STUDY OF THE BINDING OF GRAVES’ IMMUNOGLOBULINS BY THE PATIENT'S OWN AND OTHER THYROID MEMBRANES

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Abstract
Thyroid membrane preparations from 6 patients with active Graves'' disease were tested in an assay which detects the thyroid interactive Ig of Graves'' disease by their inhibition of binding of [125I]-thyroid stimulating hormone (TSH). With all preparations inhibition of binding of 125I-TSH by excess TSH could be demonstrated (specific binding). The patients'' own Ig were assayed against their own thyroid membranes and against each other''s under exactly comparable conditions. Inhibition of binding by IgG from the patients varied between membrane preparations: with 1 preparation 5/6 IgG were inhibitory but with another none were effective. Of the 6 patients, their own IgG inhibited binding of 125I-TSH to their own thyroid membrane preparation in only 4 instances, and when interaction did occur this did not reliably predict that the membrane preparation would interact with IgG from other patients with Graves'' disease. The selection of a membrane preparation for this assay cannot be made solely on ability to specifically bind TSH but the measure of the specific interaction with a Graves'' IgG of proven potency must also be considered. Because of the variability between different membrane preparations, sequential clinical studies on individual patients, of the changes in concentration of Graves'' IgG, must be performed using the same selected thyroid membrane preparation. The membrane structure in the vicinity of the TSH binding site is an important determinant of the interaction of Graves'' IgG with the TSH receptor, and the configuration of this area is variable between individuals of the same species. The distinction between human-specific and non-species-specific thyroid stimulating antibodies is therefore probably not valid. Because the patient''s own IgG was not often the most potent IgG inhibitor of binding of TSH, the Graves'' IgG binding site is apparently not identical or restricted to the TSH binding site; alternative explanations are considered.