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本文引用的文献

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Idd9.2 and Idd9.3 protective alleles function in CD4+ T-cells and nonlymphoid cells to prevent expansion of pathogenic islet-specific CD8+ T-cells.Idd9.2 和 Idd9.3 保护性等位基因在 CD4+T 细胞和非淋巴样细胞中发挥作用,以防止致病性胰岛特异性 CD8+T 细胞的扩增。
Diabetes. 2010 Jun;59(6):1478-86. doi: 10.2337/db09-1801. Epub 2010 Mar 18.
2
Predominant occupation of the class I MHC molecule H-2Kwm7 with a single self-peptide suggests a mechanism for its diabetes-protective effect.I 类 MHC 分子 H-2Kwm7 与单一自身肽优先结合,提示其具有糖尿病保护作用的机制。
Int Immunol. 2010 Mar;22(3):191-203. doi: 10.1093/intimm/dxp127. Epub 2010 Jan 21.
3
Analysis of 19 genes for association with type I diabetes in the Type I Diabetes Genetics Consortium families.1 型糖尿病遗传学联合会家族中与 1 型糖尿病相关的 19 个基因分析。
Genes Immun. 2009 Dec;10 Suppl 1(Suppl 1):S74-84. doi: 10.1038/gene.2009.96.
4
No association of the IRS1 and PAX4 genes with type I diabetes.IRS1 和 PAX4 基因与 I 型糖尿病无关。
Genes Immun. 2009 Dec;10 Suppl 1(Suppl 1):S49-53. doi: 10.1038/gene.2009.91.
5
Loss of parity between IL-2 and IL-21 in the NOD Idd3 locus.NOD Idd3基因座中IL-2与IL-21之间的失衡。
Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19438-43. doi: 10.1073/pnas.0903561106. Epub 2009 Oct 30.
6
Idd9.1 locus controls the suppressive activity of FoxP3+CD4+CD25+ regulatory T-cells.Idd9.1 基因座控制 FoxP3+CD4+CD25+调节性 T 细胞的抑制活性。
Diabetes. 2010 Jan;59(1):272-81. doi: 10.2337/db09-0648. Epub 2009 Oct 15.
7
Genetic evidence that the differential expression of the ligand-independent isoform of CTLA-4 is the molecular basis of the Idd5.1 type 1 diabetes region in nonobese diabetic mice.基因证据表明,CTLA-4配体非依赖性异构体的差异表达是非肥胖糖尿病小鼠Idd5.1型糖尿病区域的分子基础。
J Immunol. 2009 Oct 15;183(8):5146-57. doi: 10.4049/jimmunol.0802610. Epub 2009 Sep 25.
8
Thymus-specific deletion of insulin induces autoimmune diabetes.胸腺特异性胰岛素缺失会诱发自身免疫性糖尿病。
EMBO J. 2009 Sep 16;28(18):2812-24. doi: 10.1038/emboj.2009.212. Epub 2009 Aug 13.
9
Transgenic expression of single-chain anti-CTLA-4 Fv on beta cells protects nonobese diabetic mice from autoimmune diabetes.β细胞上的单链抗CTLA-4 Fv转基因表达可保护非肥胖糖尿病小鼠免受自身免疫性糖尿病的侵害。
J Immunol. 2009 Aug 15;183(4):2277-85. doi: 10.4049/jimmunol.0900679. Epub 2009 Jul 27.
10
Immune depletion with cellular mobilization imparts immunoregulation and reverses autoimmune diabetes in nonobese diabetic mice.通过细胞动员进行免疫耗竭可赋予免疫调节作用,并逆转非肥胖糖尿病小鼠的自身免疫性糖尿病。
Diabetes. 2009 Oct;58(10):2277-84. doi: 10.2337/db09-0557. Epub 2009 Jul 23.

利用非肥胖型糖尿病小鼠理解人类 1 型糖尿病。

Use of nonobese diabetic mice to understand human type 1 diabetes.

机构信息

Department of Pathology, Immunology, and Laboratory Medicine, The University of Florida College of Medicine, Gainesville, FL 32610, USA.

出版信息

Endocrinol Metab Clin North Am. 2010 Sep;39(3):541-61. doi: 10.1016/j.ecl.2010.05.001. Epub 2010 Jul 8.

DOI:10.1016/j.ecl.2010.05.001
PMID:20723819
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2925291/
Abstract

In 1922, Leonard Thompson received the first injections of insulin prepared from the pancreas of canine test subjects. From pancreatectomized dogs to the more recent development of animal models that spontaneously develop autoimmune syndromes, animal models have played a meaningful role in furthering diabetes research. Of these animals, the nonobese diabetic (NOD) mouse is the most widely used for research in type 1 diabetes (T1D) because the NOD shares several genetic and immunologic traits with the human form of the disease. In this article, the authors discuss the similarities and differences in NOD and human T1D and the potential role of NOD mice in future preclinical studies, aiming to provide a better understanding of the genetic and immune defects that lead to T1D.

摘要

1922 年,伦纳德·汤普森(Leonard Thompson)接受了首次从犬科实验对象胰腺中提取的胰岛素注射。从胰腺切除的狗到最近自发发展出自身免疫综合征的动物模型的发展,动物模型在推进糖尿病研究方面发挥了重要作用。在这些动物中,非肥胖型糖尿病(NOD)小鼠是用于 1 型糖尿病(T1D)研究最广泛的动物,因为 NOD 与人类形式的疾病具有多种遗传和免疫特征。在本文中,作者讨论了 NOD 和人类 T1D 的相似之处和不同之处,以及 NOD 小鼠在未来临床前研究中的潜在作用,旨在更好地了解导致 T1D 的遗传和免疫缺陷。