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

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          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′)<sub>2</sub>. 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.

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          Most cited references 5

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          The toxicology of iodate: a review of the literature.

          Because it is more stable than iodide, most health authorities preferentially recommend iodate as an additive to salt for correcting iodine deficiency. Even though this results in a low exposure of at most 1,700 microg/d, doubts have recently been raised whether the safety of iodate has been adequately documented. In humans and rats, oral bioavailability of iodine from iodate is virtually equivalent to that from iodide. When given intravenously to rats, or when added to whole blood or tissue homogenates in vitro or to foodstuff, iodate is quantitatively reduced to iodide by nonenzymatic reactions, and thus becomes available to the body as iodide. Therefore, except perhaps for the gastrointestinal mucosa, exposure of tissues to iodate might be minimal. At much higher doses given intravenously (i.e., above 10 mg/kg), iodate is highly toxic to the retina. Ocular toxicity in humans has occurred only after exposure to doses of 600 to 1,200 mg per individual. Oral exposures of several animal species to high doses, exceeding the human intake from fortified salt by orders of magnitude, pointed to corrosive effects in the gastrointestinal tract, hemolysis, nephrotoxicity, and hepatic injury. The studies do not meet current standards of toxicity testing, mostly because they lacked toxicokinetic data and did not separate iodate-specific effects from the effects of an overdose of any form of iodine. With regard to tissue injury, however, the data indicate a negligible risk of the small oral long-term doses achieved with iodate-fortified salt. Genotoxicity and carcinogenicity data for iodate are scarce or nonexisting. The proven genotoxic and carcinogenic effects of bromate raise the possibility of analogous activities of iodate. However, iodate has a lower oxidative potential than bromate, and it did not induce the formation of oxidized bases in DNA under conditions in which bromate did, and it may therefore present a lower genotoxic and carcinogenic hazard. This assumption needs experimental confirmation by proper genotoxicity and carcinogenicity data. These in turn will have to be related to toxicokinetic studies, which take into account the potential reduction of iodate to iodide in food, in the intestinal lumen or mucosa, or eventually during the liver passage.
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            Analysis of anti-idiotypic antibodies against anti-microsomal antibodies in patients with thyroid autoimmunity.

            Anti-microsomal antibody (AMA) activity was inhibited in 14 of 16 sera and in all 12 IgG preparations from patients with postpartum thyroiditis following incubation with F(ab')2 fragments from normal polyspecific immunoglobulin for therapeutic use (ivIg). Similar results were observed with sera from seven of seven patients with Graves' disease and five of six patients with autoimmune hypothyroidism. Results of these competitive binding assays and affinity chromatography of AMA IgG on Sepharose-bound F(ab'), fragments from ivIg indicated that AMA antibodies reacted with ivIg through idiotypic-anti-idiotypic interactions. Eight out of 10 IgG preparations from patients with autoimmune thyroid disease also showed inhibition of AMA activity when coincubated with autologous IgM at various IgG:IgM molar ratios. These observations suggest that ivIg can inhibit anti-microsomal antibodies through idiotype-anti-idiotype interactions and that such interactions occur with IgM anti-idiotype antibodies in vivo, providing evidence of a role for idiotypic network regulation in the control of thyroid autoimmunity.
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              Evidence for a Simplified View of Autoantibody Interactions with the Thyrotropin Receptor


                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                08 May 2003
                : 59
                : 5
                : 222-228
                aResearch Institute for Production Development, Shimogamo, Kyoto; bNantan General Hospital, Yagi, Kyoto; cDepartment of Radiology, Shiga University of Medical Science, Seta Otsu, Shiga, and dYamasa Ltd, Choshi, Chiba, Japan
                70221 Horm Res 2003;59:222–228
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 6, Tables: 1, References: 25, Pages: 7
                Original Paper


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