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本文引用的文献

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Oral delivery of glutamic acid decarboxylase (GAD)-65 and IL10 by Lactococcus lactis reverses diabetes in recent-onset NOD mice.通过乳球菌(Lactococcus lactis)口服传递谷氨酸脱羧酶(GAD)-65 和白细胞介素 10 可逆转近期发病的 NOD 小鼠的糖尿病。
Diabetes. 2014 Aug;63(8):2876-87. doi: 10.2337/db13-1236. Epub 2014 Mar 27.
2
1,25-Dihydroxyvitamin D3 promotes tolerogenic dendritic cells with functional migratory properties in NOD mice.1,25-二羟维生素 D3 促进 NOD 小鼠具有功能性迁移特性的耐受原性树突状细胞。
J Immunol. 2014 May 1;192(9):4210-20. doi: 10.4049/jimmunol.1302350. Epub 2014 Mar 24.
3
Discovery of molecular pathways mediating 1,25-dihydroxyvitamin D3 protection against cytokine-induced inflammation and damage of human and male mouse islets of Langerhans.发现介导 1,25-二羟维生素 D3 对抗细胞因子诱导的人及雄性小鼠胰岛炎症和损伤的分子途径。
Endocrinology. 2014 Mar;155(3):736-47. doi: 10.1210/en.2013-1409. Epub 2014 Jan 1.
4
IL-17A increases the expression of proinflammatory chemokines in human pancreatic islets.IL-17A 增加人胰岛中促炎趋化因子的表达。
Diabetologia. 2014 Mar;57(3):502-11. doi: 10.1007/s00125-013-3135-2. Epub 2013 Dec 19.
5
Candidate genes for type 1 diabetes modulate pancreatic islet inflammation and β-cell apoptosis.1 型糖尿病候选基因调节胰岛炎症和β细胞凋亡。
Diabetes Obes Metab. 2013 Sep;15 Suppl 3:71-81. doi: 10.1111/dom.12162.
6
GLIS3, a susceptibility gene for type 1 and type 2 diabetes, modulates pancreatic beta cell apoptosis via regulation of a splice variant of the BH3-only protein Bim.GLIS3 是 1 型和 2 型糖尿病的易感基因,通过调节 BH3 仅蛋白 Bim 的剪接变异体来调节胰岛β细胞凋亡。
PLoS Genet. 2013 May;9(5):e1003532. doi: 10.1371/journal.pgen.1003532. Epub 2013 May 30.
7
Regulatory multitasking of tolerogenic dendritic cells - lessons taken from vitamin d3-treated tolerogenic dendritic cells.耐受性树突状细胞的调控多任务处理 - 从维生素 D3 处理的耐受性树突状细胞中获得的经验。
Front Immunol. 2013 May 14;4:113. doi: 10.3389/fimmu.2013.00113. eCollection 2013.
8
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J Steroid Biochem Mol Biol. 2013 Jul;136:83-5. doi: 10.1016/j.jsbmb.2013.02.005. Epub 2013 Feb 13.
9
Can we vaccinate against Type 1 diabetes?我们能接种疫苗预防1型糖尿病吗?
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10
Reversal of autoimmune diabetes by restoration of antigen-specific tolerance using genetically modified Lactococcus lactis in mice.利用基因修饰的乳酸乳球菌在小鼠中恢复抗原特异性耐受逆转自身免疫性糖尿病。
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NAIMIT的故事——一个关于1型糖尿病的框架7项目。

The Story of NAIMIT - A Framework 7 Project on Type 1 Diabetes.

作者信息

Mathieu Chantal, Overbergh Lut

机构信息

Head of Endocrinology.

Senior Researcher, NAIMIT Consortium, Laboratory of Clinical and Experimental Endocrinology, KU Leuven, Leuven, Belgium.

出版信息

Eur Endocrinol. 2014 Aug;10(2):100-105. doi: 10.17925/EE.2014.10.02.100. Epub 2014 Aug 28.

DOI:10.17925/EE.2014.10.02.100
PMID:29872472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5983077/
Abstract

NAIMIT (acronym for Natural Immune Modulation for Intervention in Type 1 Diabetes) is a large-scale collaborative programme of the 7th framework from the European Commission. The aim of the consortium is to bring together a group of leading European researchers spanning the field from genetics, through pancreatic beta-cell, dendritic cells and T-cell biology, towards clinical interventions. The ultimate goal is to develop novel and personalised interventional therapies in recent-onset type 1 diabetic patients, with minimal immune system interference, leading to beta-cell protection and restoration, based on a solid understanding of the disease pathogenesis, enabling experimental findings to be adopted for clinical applications.

摘要

NAIMIT(1型糖尿病干预的自然免疫调节的首字母缩写)是欧盟委员会第七框架下的一个大规模合作项目。该联盟的目标是汇聚一批欧洲顶尖研究人员,涵盖从遗传学、胰腺β细胞、树突状细胞和T细胞生物学领域,直至临床干预。最终目标是在对疾病发病机制有深入了解的基础上,为近期发病的1型糖尿病患者开发新型个性化干预疗法,对免疫系统干扰最小,实现β细胞保护和恢复,使实验结果能够应用于临床。