The genetics of autoimmune thyroid disease.
Identifieur interne : 000017 ( Main/Exploration ); précédent : 000016; suivant : 000018The genetics of autoimmune thyroid disease.
Auteurs : Hammadi Ayadi [Tunisie] ; Hassen Hadj Kacem ; Ahmed Rebai ; Nadir R. FaridSource :
- Trends in endocrinology and metabolism: TEM [ 1043-2760 ] ; 2004.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Maladies auto-immunes.
- Cartographie chromosomique, Humains, Liaison génétique.
English descriptors
- KwdEn :
- MESH :
- genetics : Autoimmune Diseases.
- Chromosome Mapping, Genetic Linkage, Humans.
Abstract
Autoimmune thyroid diseases (AITDs), such as Graves' hyperthyroidism, are common disorders involving multiple genes and the environment. Some pathogenetic genes are probably shared between these diseases and non-endocrine autoimmune diseases, whereas others are disease specific. Population studies show that major histocompatibility complex alleles and CTLA4 confer risk for AITDs. Genetic studies have identified over 20 potential loci; only one, mapping to 5q31, has been convincingly replicated. Despite its recent emergence as an autoimmunity gatekeeper gene, linkage of CLTA4 to AITDs was described in only one Caucasian population subset. Like in the case of many complex genetic disorders, identifying AITD pathogenetic genes is limited by the ability of data analysis methods to discern the influence of genes of minor effect in a relatively small database.
DOI: 10.1016/j.tem.2004.05.002
PubMed: 15223054
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Autoimmune thyroid diseases (AITDs), such as Graves' hyperthyroidism, are common disorders involving multiple genes and the environment. Some pathogenetic genes are probably shared between these diseases and non-endocrine autoimmune diseases, whereas others are disease specific. Population studies show that major histocompatibility complex alleles and CTLA4 confer risk for AITDs. Genetic studies have identified over 20 potential loci; only one, mapping to 5q31, has been convincingly replicated. Despite its recent emergence as an autoimmunity gatekeeper gene, linkage of CLTA4 to AITDs was described in only one Caucasian population subset. Like in the case of many complex genetic disorders, identifying AITD pathogenetic genes is limited by the ability of data analysis methods to discern the influence of genes of minor effect in a relatively small database.</div>
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