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2
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本文引用的文献

1
Regulation of type 1 diabetes development and B-cell activation in nonobese diabetic mice by early life exposure to a diabetogenic environment.早年暴露于致糖尿病环境对非肥胖糖尿病小鼠1型糖尿病发展和B细胞激活的调节作用。
PLoS One. 2017 Aug 3;12(8):e0181964. doi: 10.1371/journal.pone.0181964. eCollection 2017.
2
PTPN22 and islet-specific autoimmunity: What have the mouse models taught us?蛋白酪氨酸磷酸酶非受体型22与胰岛特异性自身免疫:小鼠模型给了我们哪些启示?
World J Diabetes. 2017 Jul 15;8(7):330-336. doi: 10.4239/wjd.v8.i7.330.
3
Intestinal virome changes precede autoimmunity in type I diabetes-susceptible children.肠道病毒组变化先于 1 型糖尿病易感儿童的自身免疫。
Proc Natl Acad Sci U S A. 2017 Jul 25;114(30):E6166-E6175. doi: 10.1073/pnas.1706359114. Epub 2017 Jul 10.
4
Type 1 Diabetes and Type 1 Interferonopathies: Localization of a Type 1 Common Thread of Virus Infection in the Pancreas.1 型糖尿病与 1 型干扰素病:病毒感染在胰腺中的 1 型共同线索定位。
EBioMedicine. 2017 Aug;22:10-17. doi: 10.1016/j.ebiom.2017.06.014. Epub 2017 Jun 21.
5
CD40-mediated signalling influences trafficking, T-cell receptor expression, and T-cell pathogenesis, in the NOD model of type 1 diabetes.在1型糖尿病的非肥胖糖尿病(NOD)模型中,CD40介导的信号传导影响细胞转运、T细胞受体表达及T细胞发病机制。
Immunology. 2017 Oct;152(2):243-254. doi: 10.1111/imm.12761. Epub 2017 Jun 19.
6
Gut microbial metabolites limit the frequency of autoimmune T cells and protect against type 1 diabetes.肠道微生物代谢产物可限制自身免疫性 T 细胞的频率,并预防 1 型糖尿病。
Nat Immunol. 2017 May;18(5):552-562. doi: 10.1038/ni.3713. Epub 2017 Mar 27.
7
Islet encapsulation with polyphenol coatings decreases pro-inflammatory chemokine synthesis and T cell trafficking.用多酚涂层包裹胰岛可减少促炎趋化因子的合成和T细胞迁移。
Biomaterials. 2017 Jun;128:19-32. doi: 10.1016/j.biomaterials.2017.03.002. Epub 2017 Mar 6.
8
The common, autoimmunity-predisposing 620Arg > Trp variant of PTPN22 modulates macrophage function and morphology.常见的、自身免疫易感性的 PTPN22 620Arg>Trp 变异体调节巨噬细胞功能和形态。
J Autoimmun. 2017 May;79:74-83. doi: 10.1016/j.jaut.2017.01.009. Epub 2017 Feb 22.
9
Th40 cells (CD4+CD40+ Tcells) drive a more severe form of Experimental Autoimmune Encephalomyelitis than conventional CD4 T cells.Th40细胞(CD4+CD40+ T细胞)引发的实验性自身免疫性脑脊髓炎比传统CD4 T细胞引发的更为严重。
PLoS One. 2017 Feb 13;12(2):e0172037. doi: 10.1371/journal.pone.0172037. eCollection 2017.
10
Intestinal Epithelial Cell Regulation of Adaptive Immune Dysfunction in Human Type 1 Diabetes.肠道上皮细胞对人类1型糖尿病适应性免疫功能障碍的调节
Front Immunol. 2017 Jan 10;7:679. doi: 10.3389/fimmu.2016.00679. eCollection 2016.

新观点,基础实验(FIFE):2016年FIFE免疫学与糖尿病研讨会

Fresh Ideas, Foundational Experiments (FIFE): Immunology and Diabetes 2016 FIFE Symposium.

作者信息

Mouat Isobel C, Morse Zachary J, Jean-Baptiste Virginie S E, Allanach Jessica R, Horwitz Marc S

机构信息

Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC, Canada.

出版信息

Front Endocrinol (Lausanne). 2017 Sep 19;8:238. doi: 10.3389/fendo.2017.00238. eCollection 2017.

DOI:10.3389/fendo.2017.00238
PMID:28974943
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5610696/
Abstract

The first Fresh Ideas, Foundational Experiments (FIFE): Immunology and Diabetes symposia workshop took place in 2016 and exemplified the active interest of a number of several investigators interested the global rise in the incidence of type 1 diabetes (T1D). This increase does not correlate with genetic drift and indicates that environmental exposures are playing an increasingly significant role. Despite major biomedical and technological advances in diagnosis and treatment, treatments are frequently insufficient as they do not inhibit the progression of the underlying autoimmune response and often fail to prevent life-threatening complications. T1D is the result of autoimmune destruction of the insulin-producing beta cells of the pancreas, and the precise, mechanistic contribution of the immune system to disease pathogenesis and progression remains to be fully characterized. Ultimately, the combinatorial effect of concurrent factors, including beta cell fragility, exogenous stressors, and genetic priming of the innate and adaptive immune system, work together to induce T1D autoimmunity. Thus, T1D is the result of immunological defects and environmental pathogens, requiring the sustained attention of collaborative research teams such as FIFE: I & D with varied perspectives, unified by the universally held goal of finding a sustainable, life-long cure. Herein, the authors provide perspective on various fields in T1D research highlighted by speakers participating in the inaugural FIFE symposium.

摘要

首届“新观点、基础实验(FIFE):免疫学与糖尿病”研讨会于2016年举行,体现了众多研究人员对1型糖尿病(T1D)全球发病率上升的积极关注。这种增加与基因漂移无关,表明环境暴露正在发挥越来越重要的作用。尽管在诊断和治疗方面取得了重大的生物医学和技术进步,但治疗往往并不充分,因为它们无法抑制潜在的自身免疫反应的进展,而且常常无法预防危及生命的并发症。T1D是胰腺中产生胰岛素的β细胞发生自身免疫破坏的结果,免疫系统对疾病发病机制和进展的确切、机制性贡献仍有待充分阐明。最终,包括β细胞脆弱性、外源性应激源以及先天和适应性免疫系统的基因启动等并发因素的综合作用共同导致了T1D自身免疫。因此,T1D是免疫缺陷和环境病原体的结果,需要像FIFE:免疫学与糖尿病这样具有不同视角的合作研究团队持续关注,这些团队因寻找可持续的终身治愈方法这一共同目标而团结在一起。在此,作者提供了参与首届FIFE研讨会的演讲者所强调的T1D研究各个领域的观点。