Autoimmune Thyroid Disease Genes Come in Many Styles and Colors<sup>1</sup>

Davies, Terry F.

doi:10.1210/jcem.83.10.5253

Cited by 12 publications

(1 citation statement)

References 33 publications

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“…Данная патология характеризуется формированием нескольких вариантов, которые различаются как по функциональному состоянию ЩЖ (гипотиреоз, эутиреоз, гипертиреоз), так и её структуре (атрофия, гипертрофия, узлообразование). Исследования последних десятилетий указывают на мультифакторную природу данного заболевания [1], развивающегося в результате комплексного взаимодействия генетической предрасположенности, триггерных факторов, а также эндогенных механизмов.…”

Section: Introductionunclassified

Biochemical and immunological markers of autoimmune thyroiditis

et al. 2016

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Correlations between biochemical and immunological markers of programmed cell death (apoptosis), and the functional state of the thyroid gland (hyperthyroidism, euthyroidism, hypothyroidism) have been investigated in autoimmune thyroiditis (AT) (also known as chronic autoimmune thyroiditis). Annexin V, TRAIL and TNF-a, as well as DNA-hydrolyzing antibodies were used as the main markers. Increased levels of TRAIL were found in the serum of AT patients (hyperthyroidism>hypothyroidism>euthyroidism) compared with healthy individuals. The highest frequency of antibodies to denatured DNA (Abs-dDNA) had the highest frequency in AT patients (97%) compared with healthy controls. Among these patients, 75% had hyperthyroidism, 85% had hypothyroidism, and 84.7% had euthyroidism. Abs hydrolyzing activity demonstrated correlation dependence with symptoms of the thyroid dysfunction.

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Section: Introductionunclassified

Biochemical and immunological markers of autoimmune thyroiditis

et al. 2016

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Interleukin‐1‐β gene, but not the interleukin‐1 receptor antagonist gene, is associated with graves' disease

Chen

Chang

et al. 2005

Clinical Laboratory Analysis

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Interleukin-1 (IL-1) is considered to be involved in the pathogenesis of Graves' disease. The aim of this study was to test whether the IL-1-beta gene promoter region and exon 5 and IL-1 receptor antagonist (IL-1Ra) gene intron 2 polymorphisms could be useful genetic markers for susceptibility to Graves' disease. A normal control group of 163 healthy people and another group of 95 patients with Graves' disease were examined. Polymerase chain reaction (PCR) was used to analyze the variable number of tandem repeats (VNTRs) at intron 2 of the IL-1Ra gene for the polymorphism. PCR-based restriction analysis was done for the IL-1-beta gene polymorphisms of the promoter region and exon 5 using endonucleases AvaI and TaqI, respectively. We found significantly increased frequencies of the C/C homozygous genotype (chi(2) test, P=0.038; odds ratio (OR)=2.558, 95% confidence interval (CI)=1.205-5.430) and the C allele (chi(2) test, P=0.011; OR=1.589, 95% CI=1.094-2.309) in the IL-1-beta gene promoter (-511 C/T polymorphism) in Graves' disease patients compared to normal controls. There were no significant differences in polymorphisms of IL-1-beta gene exon 5 and IL-1Ra gene intron 2 between the patient and normal control groups. A subgroup analysis also demonstrated no association between the severity of the disease and any polymorphism of IL-1-related genes. We suggest that the IL-1-beta gene promoter polymorphism can be used as a genetic marker for susceptibility to Graves' disease. It is worthwhile to study the cytokine genes further because of the association between cytokines and Graves' disease.

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Autoimmunity in thyroid disease

Collins

Gough

2002

Eur J Nucl Med Mol Imaging

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The autoimmune thyroid diseases, Graves' disease and autoimmune hypothyroidism, represent the two ends of a disease spectrum where an immune response is directed against the thyroid gland. In Graves' disease, antibodies directed against the thyrotropin receptor (TSH-R) lead to the development of glandular overactivity, while in autoimmune hypothyroidism, cell-mediated and humoral thyroid injury leads to destruction of thyroid tissue and thyroid hormone deficiency. The mechanisms by which these diseases develop are unknown, although it is likely that both diseases occur in genetically susceptible individuals exposed to a permissive environment. A number of environmental factors have been postulated to be involved in the development of autoimmune thyroid disease. There is, however, no direct evidence to support clear causality. Susceptibility loci within immune response genes have been identified although a significant component of the genetic predisposition to disease remains unknown. This review will focus on some of the studies designed to identify genes that confer susceptibility to the autoimmune disease process within the thyroid gland.

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Autoimmune Thyroid Disease Genes Come in Many Styles and Colors¹

Cited by 12 publications

References 33 publications

Biochemical and immunological markers of autoimmune thyroiditis

Biochemical and immunological markers of autoimmune thyroiditis

Interleukin‐1‐β gene, but not the interleukin‐1 receptor antagonist gene, is associated with graves' disease

Autoimmunity in thyroid disease

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Autoimmune Thyroid Disease Genes Come in Many Styles and Colors1

Cited by 12 publications

References 33 publications

Biochemical and immunological markers of autoimmune thyroiditis

Biochemical and immunological markers of autoimmune thyroiditis

Interleukin‐1‐β gene, but not the interleukin‐1 receptor antagonist gene, is associated with graves' disease

Autoimmunity in thyroid disease

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Product

Resources

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Autoimmune Thyroid Disease Genes Come in Many Styles and Colors¹