title: In vitro suppression of anti-TSH receptor antibody by autologous anti-idiotypic antibody in patients with Graves' disease.
abstract: 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.
authors.affiliation: 3rd Department of Medicine, Kenézy Teaching Hospital, Debrecen, Hungary.
authors.forename: C
authors.initials: C
authors.lastname: Balázs
authors.forename: I
authors.initials: I
authors.lastname: Molnár
mesh_terms: D000328:Adult; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis* / Q000097:blood; D013956:Antithyroid Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000096:biosynthesis*; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D006111:Graves Disease / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology; D007074:Immunoglobulin G / Q000494:pharmacology; D007155:Immunologic Factors / Q000494:pharmacology; D066298:In Vitro Techniques; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged; D011989:Receptors, Thyrotropin / Q000276:immunology*; D013954:Thyroglobulin / Q000276:immunology; D013972:Thyrotropin / Q000276:immunology
chemical_list: D000888:Antibodies, Anti-Idiotypic; D013956:Antithyroid Agents; D001323:Autoantibodies; D007140:Immunoglobulin Fab Fragments; D007074:Immunoglobulin G; D007155:Immunologic Factors; D011989:Receptors, Thyrotropin; D008713:Methimazole; D013972:Thyrotropin; D013954:Thyroglobulin; D007453:Iodide Peroxidase