IL-2 and its high-affinity receptor: Genetic control of immunoregulation and autoimmunity

被引:47
作者
Wang, Jinguo [1 ,2 ]
Wicker, Linda S. [3 ]
Santamaria, Pere [1 ,2 ]
机构
[1] Univ Calgary, JMDRC, Fac Med, Inst Inflammat Infect & Immun, Calgary, AB T2N 4N1, Canada
[2] Univ Calgary, Dept Microbiol & Infect Dis, Fac Med, Inst Inflammat Infect & Immun, Calgary, AB T2N 4N1, Canada
[3] Univ Cambridge, Juvenile Diabet Res Fdn, Wellcome Trust Diabet & Inflammat Lab, Dept Med Genet,Cambridge Inst Med Res, Cambridge CB2 2XY, England
基金
加拿大健康研究院; 英国惠康基金;
关键词
Type; 1; diabetes; Immunogenetics; IL-2; IL-2RA; CD4+CD25+Tregs; Immunoregulation; GENOME-WIDE ASSOCIATION; REGULATORY T-CELLS; LYMPHOID TYROSINE PHOSPHATASE; TYPE-1 DIABETES LOCUS; NATURAL-KILLER-CELLS; INTERLEUKIN-2; GENE; DENDRITIC CELLS; CUTTING EDGE; ALPHA-CHAIN; RHEUMATOID-ARTHRITIS;
D O I
10.1016/j.smim.2009.04.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Type 1 diabetes (T1D) is an organ-specific autoimmune disease featured by destruction of the insulin producing beta-cells of the pancreas by autoreactive T-lymphocytes. Putative environmental triggers conspire with a constellation of genetic elements scattered throughout the genome to elicit a multifactorial autoimmune response involving virtually every cell type of the immune system against pancreatic beta-cells. Recent highly powered genome-wide association studies have confirmed and identified fifteen chromosomal regions harboring several candidate T1D-associated gene loci. Here, we summarize what we know about the genetics of T1D with an emphasis on the contributions of mouse IL2 and human IL2RA polymorphisms and the IL-2-IL-2R pathway to autoimmunity and, more specifically, Treg development and function. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:363 / 371
页数:9
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