Graves Disease

Menconi, Francesca; Oppenheim, Yael L.; Tomer, Yaron

doi:10.1007/978-1-60327-285-8_44

Cited by 29 publications

(19 citation statements)

References 8 publications

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“…GD is defined by the presence of stimulating TSHR antibodies (4). Not surprisingly, the TSHR was the first gene (after HLA) to be tested for association with GD.…”

Section: Thyroid-specific Genesmentioning

confidence: 99%

“…In HT the lymphocytic infiltration of the thyroid gland leads to apoptosis of thyroid cells and hypothyroidism (3). In contrast, in GD the lymphocytic infiltration of the thyroid leads to activation of thyrotropin receptor (TSHR)-reactive B-cells that secrete TSHR-stimulating antibodies causing hyperthyroidism (4). The etiology of HT and GD involves common pathways in which thyroid reactive T-cells escape tolerance and infiltrate the thyroid, and unique pathways in which these thyroid-reactive T-cells either cause thyroid cell death (in HT) or stimulation (in GD).…”

Section: Introductionmentioning

confidence: 96%

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Genetic Susceptibility to Autoimmune Thyroid Disease: Past, Present, and Future

Tomer

2010

Thyroid

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188

133

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“…GD is defined by the presence of stimulating TSHR antibodies (4). Not surprisingly, the TSHR was the first gene (after HLA) to be tested for association with GD.…”

Section: Thyroid-specific Genesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Genetic Susceptibility to Autoimmune Thyroid Disease: Past, Present, and Future

Tomer

2010

Thyroid

Self Cite

188

133

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“…The two major autoimmune thyroid diseases (AITD) include Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), both of which are characterized pathologically by infiltration of the thyroid by T and B cells, reactive to thyroid antigens, biochemically by the production of thyroid autoantibodies, and clinically by abnormal thyroid functions (hyperthyroidism in GD and hypothyroidism in HT) (reviewed in (1; 2)). Additional variants of AITD include post-partum thyroiditis (reviewed in (3–5)), drug induced thyroiditis, such as interferon induced thyroiditis (IIT) (6), thyroiditis associated with polyglandular autoimmune syndromes (reviewed in (7; 8).…”

Section: Introductionmentioning

confidence: 99%

The etiology of autoimmune thyroid disease: A story of genes and environment

Tomer

Huber

2009

Journal of Autoimmunity

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310

232

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Autoimmune thyroid diseases (AITD), including Graves’ disease (GD) and Hashimoto’s thyroiditis (HT) are prevalent autoimmune diseases, affecting up to 5% of the general population. Autoimmune thyroid diseases arise due to complex interactions between environmental and genetic factors. Significant progress has been made in our understanding of the genetic and environmental triggers contributing to AITD. However, the interactions between genes and environment are yet to be defined. Among the major AITD susceptibility genes that have been identified and characterized is the HLADR gene locus, as well as non-MHC genes including the CTLA-4, CD40, PTPN22, thyroglobulin, and TSH receptor genes. The major environmental triggers of AITD include iodine, medications, infection, smoking, and possibly stress. Recent data on the genetic predisposition to AITD lead to novel putative mechanisms by which the genetic-environmental interactions may lead to the development of thyroid autoimmunity.

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“…Autoimmune thyroid diseases (AITDs), such as Graves' disease (GD) and Hashimoto's disease (HD), are typical autoimmune diseases [1,2]. The severity of HD and the intractability (that is, inducibility to remission) of GD varies among patients.…”

Section: Introductionmentioning

confidence: 99%

Association of polymorphisms in DNMT1, DNMT3A, DNMT3B, MTHFR and MTRR genes with global DNA methylation levels and prognosis of autoimmune thyroid disease

Arakawa¹,

Watanabe²,

Inoue³

et al. 2012

Clinical and Experimental Immunology

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SummaryTo clarify the association between factors regulating DNA methylation and the prognosis of autoimmune thyroid diseases (AITDs), we genotyped single nucleotide polymorphisms in genes encoding DNA methyltransferase 1 (DNMT1), DNMT3A, DNMT3B, methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR), which are enzymes essential for DNA methylation. Subjects for this study included 125 patients with Hashimoto's disease (HD), including 48 patients with severe HD and 49 patients with mild HD; 176 patients with Graves' disease (GD), including 79 patients with intractable GD and 47 patients with GD in remission; and 83 healthy volunteers (control subjects). The DNMT1 +32204GG genotype was more frequent in patients with intractable GD than in patients with GD in remission. Genomic DNA showed significantly lower levels of global methylation in individuals with the DNMT1 +32204GG genotype than in those with the AA genotype. The MTRR +66AA genotype was observed to be more frequent in patients with severe HD than in those with mild HD. The DNMT1 +14395A/G, DNMT3B -579G/T, MTHFR +677C/T and +1298A/C polymorphisms were not correlated with the development or prognosis of AITD. Our study indicates that the DNMT1 +32204GG genotype correlates with DNA hypomethylation and with the intractability of GD, and that the MTRR +66AA genotype may correlate with the severity of HD.

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Graves Disease

Cited by 29 publications

References 8 publications

Genetic Susceptibility to Autoimmune Thyroid Disease: Past, Present, and Future

Genetic Susceptibility to Autoimmune Thyroid Disease: Past, Present, and Future

The etiology of autoimmune thyroid disease: A story of genes and environment

Association of polymorphisms in DNMT1, DNMT3A, DNMT3B, MTHFR and MTRR genes with global DNA methylation levels and prognosis of autoimmune thyroid disease

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