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

被引：81

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

来源：

SEMINARS IN IMMUNOLOGY | 2009年 / 21卷 / 06期

基金：

英国惠康基金; 加拿大健康研究院;

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：

071005 [微生物学]; 100108 [医学免疫学];

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

页码：363 / 371

页数：9

共 123 条

[1]

Cell-type-specific epigenetic marking of the IL2 gene at a distal cis-regulatory region in competent, nontranscribing T-cells [J].