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There are sound data coming from epidemiological, family, and twin studies demonstrating a strong genetic influence on the development of AITD. In this review we summarize the new findings on the genetic susceptibility to AITD focusing on emerging mechanisms of susceptibility.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Summary:<\/jats:title>\n                    <jats:p>\n                      Candidate gene analysis, whole-genome linkage screening, genome-wide association studies, and whole-genome sequencing are the major technologies that have advanced this field, leading to the identification of at least seven genes whose variants have been associated with AITD. One of the major ones is the\n                      <jats:italic toggle=\"yes\">HLA-DR<\/jats:italic>\n                      gene locus. Recently, it was shown that substitution of the neutral amino acids Ala or Gln with arginine at position beta 74 in the\n                      <jats:italic toggle=\"yes\">HLA-DR<\/jats:italic>\n                      peptide-binding pocket is key to the etiology of both Graves' disease and Hashimoto's thyroiditis. Several other genes have also been shown to confer susceptibility to AITD. These can be classified into two groups: (i) immune regulatory genes (cytotoxic T lymphocyte-associated protein 4,\n                      <jats:italic toggle=\"yes\">CD40<\/jats:italic>\n                      , protein tyrosine phosphatase-22, and\n                      <jats:italic toggle=\"yes\">CD25<\/jats:italic>\n                      ) and (ii) thyroid-specific genes (thyroglobulin and thyrotropin receptor genes). The influence of individual genes on the development of AITD when assessed in a population appears to be weaker than would be expected from the data showing strong genetic susceptibility to AITD. Two possible mechanisms explaining this discrepancy are gene\u2013gene interactions and subset effects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Significant progress has been made in our understanding of the immunogenetic mechanisms leading to thyroid autoimmunity. For the first time we are beginning to unravel these mechanisms at the molecular level. It is hoped that these new data will be translated into novel therapies and prevention strategies in AITD, such as costimulatory blockade.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/thy.2010.1644","type":"journal-article","created":{"date-parts":[[2010,7,6]],"date-time":"2010-07-06T13:19:25Z","timestamp":1278422365000},"page":"715-725","source":"Crossref","is-referenced-by-count":176,"title":["Genetic Susceptibility to Autoimmune Thyroid Disease: Past, Present, and Future"],"prefix":"10.1177","volume":"20","author":[{"given":"Yaron","family":"Tomer","sequence":"first","affiliation":[{"name":"Mount Sinai Medical Center"},{"name":"Bronx VA Medical Center"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2010,7]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1210\/er.2008-0015"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1006\/clin.1997.4412"},{"key":"e_1_3_3_4_2","first-page":"721","volume-title":"Werner and Ingbar's The Thyroid","author":"Weetman AP","year":"2000","unstructured":"Weetman AP. 2000. 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