THE PUTATIVE ANTI‐THYROTROPIN RECEPTOR ANTIBODIES OF GRAVES' DISEASE:I. Gm ALLOTYPES *

Pepper, Barbara; Noel, Elke P.; Farid, Nadir R.

doi:10.1111/j.1744-313x.1981.tb00746.x

Cited by 14 publications

(4 citation statements)

References 39 publications

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“…We also found a modest increase in fb homozygotes (R.R. N 2.5) among the seventy patients with Graves' disease previously studied (Farid et al, 1977;Pepper et al, 1981). In contrast to the patients with thyroiditis, however, patients with Graves' disease show a far greater increase in fb haplotypes.…”

Section: Discussionsupporting

confidence: 51%

IgG HEAVY CHAIN ALLOTYPES (Gm) IN ATROPHIC AND GOITROUS THYROIDITIS

Nakao

Matsumoto

Miyazaki

et al. 1982

Int J Immunogenetics

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SUMMARY We typed coded sera from 135 healthy controls, seventy‐six patients with autoimmne goitrous and seventy‐three with atrophic thyroiditis for IgG heavy chain markers (Gm). All subjects were Caucasian from Newfoundland. An increase in the Gm phenotype ag was found in the 149 patients with thyroiditis compared to controls (X12= 5.82, P <0.01); significance was, however, not maintained after correction for the number of variables tested. The difference in ag phenotype was more pronounced among the seventy‐three patients with atrophic thyroiditis (X12= 8.80 corrected P < 0.05). Because the haplotype ag was not significantly increased in this group, we conclude that homozygotes for Gm ag are at an increased risk of developing atrophic thyroiditis.

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Section: Discussionsupporting

confidence: 51%

IgG HEAVY CHAIN ALLOTYPES (Gm) IN ATROPHIC AND GOITROUS THYROIDITIS

Nakao

Matsumoto

Miyazaki

et al. 1982

Int J Immunogenetics

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“…In most hyperthyroid Graves' patients it is reasonable to assume that such TSH-receptor antibodies are responsible for the thyroidal hyperfunction and are the same antibodies as measured by a variety of bioassays for thyroid-stimulators (Zakarija & McKenzie, 1980a). Evidence of antibody restriction in Graves' IgG containing thyroid-stimulating antibodies (TSAb) adds weight to this logical assumption (Zakarija & McKenzie, 1980b;Pepper et al, 1981).…”

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confidence: 99%

Prediction of Therapeutic Response to Radioactive Iodine in Graves’disease Using Tsh‐receptor Antibodies and Hla‐status

Davies

Platzer

Farid

1982

Clinical Endocrinology

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We have examined the combined usefulness of TSH-receptor antibody detection and HLA status on the therapeutic response to standard doses of radioactive iodine (RAI) in forty-three hyperthyroid Graves' patients. Twenty-three patients had detectable TSH-receptor antibodies as measured by 125I-TSH binding-inhibition (TBI) prior to administration of 7 mCi RAI. Eighteen (78%) of these patients were rendered euthyroid within 3 months. In contrast, twenty patients were TBI negative prior to RAI and sixteen (80%) of these individuals remained hyperthyroid at 3 months and required two, or more, doses of RAI to control their thyroid function. DR3 status alone was not strongly associated with resistance to RAI. However, of sixteen patients without detectable TBI activity and who required two or more doses of RAI, ten patients were DR3 positive (62%) compared with 25% in a control population. Only one patient who was both TBI and DR3 negative required more than one dose of RAI. These data indicate that TBI may be an accurate predictor of the therapeutic response to RAI in patients with hyperthyroid Graves' disease. Investigation of HLA status alone was of limited value, although it appeared that the combination of TBI and DR3 may be of additional help in developing an overall strategy for the treatment of hyperthyroid Graves' disease.

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“…Graves' disease is an exclusively human pathology and there are no spontaneous or induced experimental animal models. There is some evidence that Graves' disease is linked with certain Ig allotypes and in familial studies of affected members there is allotype sharing [65,71,91,100]. There is an association with DR3 and DR5 in caucasians [84,92] but not in American blacks [85], whereas HLA-Bw45 is associated with Graves' disease in Japanese populations [15], although the relative risk factors are low.…”

Section: Graves' Diseasementioning

confidence: 99%

Autoantigens in thyroid diseases

Dawe

Hutchings

Champion

et al. 1993

Springer Semin Immunopathol

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The autoantigens involved in autoimmune thyroid disease have now been extensively characterised, and the autoantibodies they evoke provide important aids to diagnosis, leading to early treatment of thyroid autoimmunity. The next stage in the puzzle is to determine towards which epitopes on the autoantigens the immune response is directed. We have already come a long way in the identification of immunodominant epitopes and have been able to identify one T cell epitope which has pathogenic capabilities. Identification of other T cell and B cell epitopes will help us understand the cell-mediated and humoral responses in greater detail and in time lead to more specific therapeutic intervention. A greater understanding of the mechanisms underlying one particular autoimmune disease will give us insights into other diseases, due to the belief that there may well be common underlying defects that, due to a multitude of factors, manifest as different diseases. The susceptibility factors in autoimmune thyroidits and autoimmune disease in general are very complex. A greater understanding is required of HLA associations and how particular peptides are presented in vivo. Are susceptible MHC types the ones capable of presenting the pathogenic peptides? Our major T cell thyroiditogenic epitope contains a T4 residue which accounts for over half the molecular weight of the peptide. Its structure is large and consists of a double benzene ring structure with four iodine atoms. It will be interesting to see how such a peptide can be presented and which residues bind T cell receptor or MHC. In summary we can say that autoimmune disease is due to a cocktail of factors which all contrive to tip the delicate balance of the immune system into an autoimmune state. HLA association may play a role in conferring an enhanced ability to select from a restricted repertoire of pathogenic epitopes, those epitopes perhaps only becoming available for presentation after interaction with environmental agents, whatever they may be. Following this, the normal regulation of self presentation and tolerance mechanisms break down and autoimmunity supervenes.

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THE PUTATIVE ANTI‐THYROTROPIN RECEPTOR ANTIBODIES OF GRAVES' DISEASE:I. Gm ALLOTYPES *

Cited by 14 publications

References 39 publications

IgG HEAVY CHAIN ALLOTYPES (Gm) IN ATROPHIC AND GOITROUS THYROIDITIS

IgG HEAVY CHAIN ALLOTYPES (Gm) IN ATROPHIC AND GOITROUS THYROIDITIS

Prediction of Therapeutic Response to Radioactive Iodine in Graves’disease Using Tsh‐receptor Antibodies and Hla‐status

Autoantigens in thyroid diseases

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