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本文引用的文献

1
Human enterovirus infections in children at increased risk for type 1 diabetes: the Babydiet study.儿童人类肠道病毒感染与 1 型糖尿病风险增加:Babydiet 研究。
Diabetologia. 2011 Dec;54(12):2995-3002. doi: 10.1007/s00125-011-2305-3. Epub 2011 Sep 20.
2
Vaccine-derived poliomyelitis 12 years after infection in Minnesota.明尼苏达州感染后 12 年出现疫苗衍生脊髓灰质炎
N Engl J Med. 2011 Jun 16;364(24):2316-23. doi: 10.1056/NEJMoa1008677.
3
Enterovirus infection and type 1 diabetes mellitus: systematic review and meta-analysis of observational molecular studies.肠道病毒感染与 1 型糖尿病:观察性分子研究的系统评价和荟萃分析。
BMJ. 2011 Feb 3;342:d35. doi: 10.1136/bmj.d35.
4
Genetics of type 1 diabetes.1 型糖尿病的遗传学。
Clin Chem. 2011 Feb;57(2):176-85. doi: 10.1373/clinchem.2010.148221. Epub 2011 Jan 4.
5
Enterovirus RNA in blood is linked to the development of type 1 diabetes.血液中的肠道病毒 RNA 与 1 型糖尿病的发生有关。
Diabetes. 2011 Jan;60(1):276-9. doi: 10.2337/db10-0186. Epub 2010 Oct 13.
6
Enterovirus infection and progression from islet autoimmunity to type 1 diabetes: the Diabetes and Autoimmunity Study in the Young (DAISY).肠道病毒感染与胰岛自身免疫向 1 型糖尿病的进展:青年糖尿病与自身免疫研究(DAISY)。
Diabetes. 2010 Dec;59(12):3174-80. doi: 10.2337/db10-0866. Epub 2010 Sep 21.
7
Evidence for molecular mimicry between human T cell epitopes in rotavirus and pancreatic islet autoantigens.轮状病毒与人 T 细胞表位和胰腺胰岛自身抗原之间存在分子模拟的证据。
J Immunol. 2010 Feb 15;184(4):2204-10. doi: 10.4049/jimmunol.0900709. Epub 2010 Jan 18.
8
T cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous event.1型糖尿病中T细胞在胰岛的积聚是一个受到严格调控的细胞自主事件。
Immunity. 2009 Oct 16;31(4):643-53. doi: 10.1016/j.immuni.2009.07.008. Epub 2009 Oct 8.
9
Rheumatic fever and rheumatic heart disease: cellular mechanisms leading autoimmune reactivity and disease.风湿热和风湿性心脏病:导致自身免疫反应和疾病的细胞机制。
J Clin Immunol. 2010 Jan;30(1):17-23. doi: 10.1007/s10875-009-9332-6. Epub 2009 Oct 3.
10
No effect of the altered peptide ligand NBI-6024 on beta-cell residual function and insulin needs in new-onset type 1 diabetes.新型 1 型糖尿病中,改变的肽配体 NBI-6024 对β细胞残余功能和胰岛素需求没有影响。
Diabetes Care. 2009 Nov;32(11):2036-40. doi: 10.2337/dc09-0449. Epub 2009 Aug 18.

病毒感染与 1 型糖尿病中的分子模拟。

Viral infections and molecular mimicry in type 1 diabetes.

机构信息

Type 1 Diabetes Center, The La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.

出版信息

APMIS. 2012 Dec;120(12):941-9. doi: 10.1111/apm.12011. Epub 2012 Oct 11.

DOI:10.1111/apm.12011
PMID:23051179
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5774991/
Abstract

Type 1 diabetes (T1D) is a disease characterized by inflammation of pancreatic islets associated with autoimmunity against insulin-producing beta cells, leading to their progressive destruction. The condition constitutes a significant and worldwide problem to human health, particularly because of its rapid, but thus far unexplained, increase in incidence. Environmental factors such as viral infections are thought to account for this trend. While there is no lack of reports associating viral infections toT1D, it has proven difficult to establish which immunological processes link viral infections to disease onset or progression. One of the commonly discussed pathways is molecular mimicry, a mechanism that encompasses cross-reactive immunity against epitopes shared between viruses and beta cells. In this review, we will take a closer look at mechanistic evidence for a potential role of viruses in T1D, with a special focus on molecular mimicry.

摘要

1 型糖尿病(T1D)是一种以胰岛炎症为特征的疾病,其与针对产生胰岛素的β细胞的自身免疫有关,导致β细胞的进行性破坏。这种疾病对人类健康构成了重大的全球性问题,尤其是因为其发病率迅速上升,但目前仍不清楚其原因。人们认为环境因素,如病毒感染,是造成这种趋势的原因。虽然有很多报告将病毒感染与 T1D 联系起来,但要确定哪些免疫过程将病毒感染与疾病的发生或进展联系起来,这一直是个难题。其中一个被广泛讨论的途径是分子模拟,这是一种机制,包括病毒和β细胞之间共享表位的交叉反应性免疫。在这篇综述中,我们将更仔细地研究病毒在 T1D 中可能发挥作用的机制证据,特别关注分子模拟。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40d6/5774991/edd2c4577454/nihms916902f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40d6/5774991/177cd3a3da02/nihms916902f1.jpg
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