Abstract
The autoimmune thyroid diseases (AITD) include Graves disease (GD) and Hashimotos thyroiditis (HT), which are characterised by a breakdown in immune tolerance to thyroid antigens. Unravelling the genetic architecture of AITD is vital to better understanding of AITD pathogenesis, required to advance therapeutic options in both disease management and prevention. The early whole-genome linkage and candidate gene association studies provided the first evidence that the HLA region and CTLA-4 represented AITD risk loci. Recent improvements in; high throughput genotyping technologies, collection of larger disease cohorts and cataloguing of genome-scale variation have facilitated genome-wide association studies and more thorough screening of candidate gene regions. This has allowed identification of many novel AITD risk genes and more detailed association mapping. The growing number of confirmed AITD susceptibility loci, implicates a number of putative disease mechanisms most of which are tightly linked with aspects of immune system function. The unprecedented advances in genetic study will allow future studies to identify further novel disease risk genes and to identify aetiological variants within specific gene regions, which will undoubtedly lead to a better understanding of AITD patho-physiology.
Keywords: Autoimmune thyroid disease, Graves' disease, association, genes, Hashimoto's thyroiditis, Multiple sclerosis, GWAS, TSHR, meta-analysis, T lymphocytes
Current Genomics
Title: Immunogenetic Mechanisms Leading to Thyroid Autoimmunity: Recent Advances in Identifying Susceptibility Genes and Regions
Volume: 12 Issue: 8
Author(s): Oliver J. Brand and Stephen C.L. Gough
Affiliation:
Keywords: Autoimmune thyroid disease, Graves' disease, association, genes, Hashimoto's thyroiditis, Multiple sclerosis, GWAS, TSHR, meta-analysis, T lymphocytes
Abstract: The autoimmune thyroid diseases (AITD) include Graves disease (GD) and Hashimotos thyroiditis (HT), which are characterised by a breakdown in immune tolerance to thyroid antigens. Unravelling the genetic architecture of AITD is vital to better understanding of AITD pathogenesis, required to advance therapeutic options in both disease management and prevention. The early whole-genome linkage and candidate gene association studies provided the first evidence that the HLA region and CTLA-4 represented AITD risk loci. Recent improvements in; high throughput genotyping technologies, collection of larger disease cohorts and cataloguing of genome-scale variation have facilitated genome-wide association studies and more thorough screening of candidate gene regions. This has allowed identification of many novel AITD risk genes and more detailed association mapping. The growing number of confirmed AITD susceptibility loci, implicates a number of putative disease mechanisms most of which are tightly linked with aspects of immune system function. The unprecedented advances in genetic study will allow future studies to identify further novel disease risk genes and to identify aetiological variants within specific gene regions, which will undoubtedly lead to a better understanding of AITD patho-physiology.
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Cite this article as:
J. Brand Oliver and C.L. Gough Stephen, Immunogenetic Mechanisms Leading to Thyroid Autoimmunity: Recent Advances in Identifying Susceptibility Genes and Regions, Current Genomics 2011; 12 (8) . https://dx.doi.org/10.2174/138920211798120790
DOI https://dx.doi.org/10.2174/138920211798120790 |
Print ISSN 1389-2029 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5488 |
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