NOD小鼠中HLA-DQ8转基因且缺乏I-Ag7时的胰岛细胞自身免疫。 - Suppr

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超能文献

Islet cell autoimmunity in NOD mice transgenic for HLA-DQ8 and lacking I-Ag7.

作者信息

Raju R, Munn S R, Majoribanks C, David C S

机构信息

Department of Immunology and Transplantation, Mayo Clinic, Rochester, Minnesota, USA.

出版信息

Transplant Proc. 1998 Mar;30(2):561. doi: 10.1016/s0041-1345(97)01404-8.

DOI:10.1016/s0041-1345(97)01404-8

PMID:9532176

Abstract

摘要

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Islet cell autoimmunity in NOD mice transgenic for HLA-DQ8 and lacking I-Ag7.NOD小鼠中HLA-DQ8转基因且缺乏I-Ag7时的胰岛细胞自身免疫。

Transplant Proc. 1998 Mar;30(2):561. doi: 10.1016/s0041-1345(97)01404-8.

Islet cell autoimmunity in NOD mice transgenic to HLA-DQ8 and lacking I-Ag7.转HLA - DQ8基因且缺乏I - Ag7的非肥胖糖尿病（NOD）小鼠中的胰岛细胞自身免疫。

Transplant Proc. 1998 Mar;30(2):474. doi: 10.1016/s0041-1345(97)01362-6.

Human DQ8 can substitute for murine I-Ag7 in the selection of diabetogenic T cells restricted to I-Ag7.人类DQ8可替代小鼠I-Ag7，用于选择受I-Ag7限制的致糖尿病T细胞。

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[Mechanism and genetic control of the autoimmune response directed against beta-pancreatic cells in insulin-dependent diabetes].[胰岛素依赖型糖尿病中针对β胰腺细胞的自身免疫反应的机制与遗传控制]

Journ Annu Diabetol Hotel Dieu. 1985:171-82.

Major DQ8-restricted T-cell epitopes for human GAD65 mapped using human CD4, DQA1*0301, DQB1*0302 transgenic IA(null) NOD mice.使用人CD4、DQA1*0301、DQB1*0302转基因IA（无）NOD小鼠定位人GAD65的主要DQ8限制性T细胞表位。

Diabetes. 1999 Mar;48(3):469-77. doi: 10.2337/diabetes.48.3.469.

The murine diabetogenic class II histocompatibility molecule I-Ag7: structural and functional properties and specificity of peptide selection.小鼠致糖尿病性II类组织相容性分子I-Ag7：肽段选择的结构与功能特性及特异性

Adv Immunol. 2005;88:235-65. doi: 10.1016/S0065-2776(05)88007-1.

NOD background genes influence T cell responses to GAD 65 in HLA-DQ8 transgenic mice.非肥胖糖尿病（NOD）背景基因影响HLA-DQ8转基因小鼠中T细胞对谷氨酸脱羧酶65（GAD 65）的反应。

Hum Immunol. 1999 Jul;60(7):583-90. doi: 10.1016/s0198-8859(99)00057-9.

Prevention of diabetes in NOD mice by a mutated I-Ab transgene.通过突变的I-Ab转基因预防非肥胖糖尿病（NOD）小鼠患糖尿病。

Diabetes. 1998 Oct;47(10):1570-7. doi: 10.2337/diabetes.47.10.1570.

I-Ag7-mediated antigen presentation by B lymphocytes is critical in overcoming a checkpoint in T cell tolerance to islet beta cells of nonobese diabetic mice.I-Ag7介导的B淋巴细胞抗原呈递对于克服非肥胖糖尿病小鼠T细胞对胰岛β细胞耐受性的一个检查点至关重要。

J Immunol. 1999 Jul 15;163(2):743-50.

Induction of insulitis by glutamic acid decarboxylase peptide-specific and HLA-DQ8-restricted CD4(+) T cells from human DQ transgenic mice.来自人DQ转基因小鼠的谷氨酸脱羧酶肽特异性且受HLA-DQ8限制的CD4(+) T细胞诱导胰岛炎

J Clin Invest. 1998 Sep 1;102(5):947-57. doi: 10.1172/JCI2723.

引用本文的文献

The importance of the Non Obese Diabetic (NOD) mouse model in autoimmune diabetes.非肥胖糖尿病（NOD）小鼠模型在自身免疫性糖尿病中的重要性。

J Autoimmun. 2016 Jan;66:76-88. doi: 10.1016/j.jaut.2015.08.019. Epub 2015 Sep 26.

A new model defines the minimal set of polymorphism in HLA-DQ and -DR that determines susceptibility and resistance to autoimmune diabetes.一种新模型定义了HLA-DQ和-DR中多态性的最小集合，该集合决定了对自身免疫性糖尿病的易感性和抗性。

Biol Direct. 2008 Oct 14;3:42. doi: 10.1186/1745-6150-3-42.

Natural peptides selected by diabetogenic DQ8 and murine I-A(g7) molecules show common sequence specificity.由致糖尿病的DQ8和小鼠I-A(g7)分子选择的天然肽显示出共同的序列特异性。

J Clin Invest. 2005 Aug;115(8):2268-76. doi: 10.1172/JCI25350.

HLA-DQ polymorphism influences progression of demyelination and neurologic deficits in a viral model of multiple sclerosis.HLA-DQ基因多态性影响多发性硬化病毒模型中脱髓鞘进展和神经功能缺损。

Mol Cell Neurosci. 2000 Jun;15(6):495-509. doi: 10.1006/mcne.2000.0843.

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