Influence of Type 1 Diabetes Genes on Disease Progression: Similarities and Differences Between Countries

被引：6

作者：

Lempainen, Johanna ^{[1
,2
,3
]}

Ilonen, Jorma ^{[1
,4
]}

机构：

[1] Univ Turku, Immunogenet Lab, FIN-20520 Turku, Finland

[2] Univ Turku, Dept Pediat, FIN-20520 Turku, Finland

[3] Turku Univ Hosp, Dept Pediat, FIN-20520 Turku, Finland

[4] Univ Eastern Finland, Dept Clin Microbiol, Kuopio, Finland

来源：

CURRENT DIABETES REPORTS | 2012年 / 12卷 / 05期

基金：

芬兰科学院;

关键词：

Type; 1; diabetes; Disease progression; Genes; HLA; PTPN22; IFIH1; BETA-CELL AUTOIMMUNITY; HLA CLASS-I; LYMPHOID TYROSINE PHOSPHATASE; GENOME-WIDE ASSOCIATION; ISLET AUTOANTIBODIES; CESAREAN-SECTION; MELLITUS IDDM; INSULIN GENE; HUMAN THYMUS; RISK;

D O I：

10.1007/s11892-012-0310-7

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Type 1 diabetes (T1D) is an autoimmune disease causing the destruction of pancreatic beta cells. The onset of clinical T1D is preceded by a time period called pre-diabetes, the duration of which varies widely. However, not all subjects developing beta-cell autoimmunity progress to clinical T1D. The inherited risk for T1D is determined by the human leukocyte antigen (HLA) class II genes, HLA class I genes, and several loci outside the HLA area. Although the role of the genetic risk variants in disease pathogenesis is not completely understood, some of the variants affecting disease risk are thought to influence the initiation of beta-cell autoimmunity whereas others seem to play a role during the later stages of the autoimmune process. In this review we describe the current knowledge on the genetic factors mediating the fate of already-established beta-cell autoimmunity and the rate of beta-cell destruction.

引用

页码：447 / 455

页数：9

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