Type 1 diabetes and polyglandular autoimmune syndrome: A review
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  • 英文篇名:Type 1 diabetes and polyglandular autoimmune syndrome: A review
  • 作者:Martin ; P ; Hansen ; Nina ; Matheis ; George ; J ; Kahaly
  • 英文作者:Martin P Hansen;Nina Matheis;George J Kahaly;Department of Medicine I, Johannes Gutenberg University Medical Center;
  • 英文关键词:Autoimmune thyroid disease;;Polyglandular autoimmune syndrome;;Addison's disease;;Susceptibility genes;;Type 1 diabetes
  • 中文刊名:WJDE
  • 英文刊名:世界糖尿病杂志(电子版)(英文版)
  • 机构:Department of Medicine I, Johannes Gutenberg University Medical Center;
  • 出版日期:2015-02-15
  • 出版单位:World Journal of Diabetes
  • 年:2015
  • 期:v.6
  • 语种:英文;
  • 页:WJDE201501007
  • 页数:13
  • CN:01
  • 分类号:76-88
摘要
Type 1 diabetes(T1D) is an autoimmune disorder caused by inflammatory destruction of the pancreatic tissue. The etiopathogenesis and characteristics of the pathologic process of pancreatic destruction are well described. In addition, the putative susceptibility genes for T1 D as a monoglandular disease and the relation to polyglandular autoimmune syndrome(PAS) have also been wellexplored. The incidence of T1 D has steadily increased in most parts of the world, especially in industrialized nations. T1 D is frequently associated with autoimmune endocrine and non-endocrine diseases and patients with T1 D are at a higher risk for developing several glandular autoimmune diseases. Familial clustering is observed, which suggests that there is a genetic predisposition. Various hypotheses pertaining to viral- and bacterialinduced pancreatic autoimmunity have been proposed, however a definitive delineation of the autoimmune pathomechanism is still lacking. In patients with PAS, pancreatic and endocrine autoantigens either colocalize on one antigen-presenting cell or are expressed on two/various target cells sharing a common amino acid, which facilitates binding to and activation of T cells. The most prevalent PAS phenotype is the adult type 3 variant or PAS type Ⅲ, which encompasses T1 D and autoimmune thyroid disease. This review discusses the findings of recent studies showing noticeable differences in the genetic background and clinical phenotype of T1 D either as an isolated autoimmune endocrinopathy or within the scope of polyglandular autoimmune syndrome.
        Type 1 diabetes(T1D) is an autoimmune disorder caused by inflammatory destruction of the pancreatic tissue. The etiopathogenesis and characteristics of the pathologic process of pancreatic destruction are well described. In addition, the putative susceptibility genes for T1 D as a monoglandular disease and the relation to polyglandular autoimmune syndrome(PAS) have also been wellexplored. The incidence of T1 D has steadily increased in most parts of the world, especially in industrialized nations. T1 D is frequently associated with autoimmune endocrine and non-endocrine diseases and patients with T1 D are at a higher risk for developing several glandular autoimmune diseases. Familial clustering is observed, which suggests that there is a genetic predisposition. Various hypotheses pertaining to viral- and bacterialinduced pancreatic autoimmunity have been proposed, however a definitive delineation of the autoimmune pathomechanism is still lacking. In patients with PAS, pancreatic and endocrine autoantigens either colocalize on one antigen-presenting cell or are expressed on two/various target cells sharing a common amino acid, which facilitates binding to and activation of T cells. The most prevalent PAS phenotype is the adult type 3 variant or PAS type Ⅲ, which encompasses T1 D and autoimmune thyroid disease. This review discusses the findings of recent studies showing noticeable differences in the genetic background and clinical phenotype of T1 D either as an isolated autoimmune endocrinopathy or within the scope of polyglandular autoimmune syndrome.
引文
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