肠病毒与1型糖尿病:多重机制和因素?

IF 15.1 1区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL Annual review of medicine Pub Date : 2022-01-27 DOI:10.1146/annurev-med-042320-015952
Richard E Lloyd, Manasi Tamhankar, Åke Lernmark
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引用次数: 23

摘要

1型糖尿病(T1D)是一种以胰岛素缺乏和由此产生的高血糖为特征的慢性自身免疫性疾病。遗传和环境因素的复杂相互作用触发自身免疫机制的启动,负责对β细胞抗原的自身免疫的发展和随后的T1D的发展。长期以来,人们一直假设病毒感染的潜在作用,越来越多的证据继续表明肠病毒是最可能的触发病毒。最近的研究加强了肠道病毒与T1D患者自身免疫发展之间的联系,可能通过持续感染。肠道病毒感染可能导致疾病发展的不同阶段。我们回顾了人类队列研究和实验研究的数据,探索肠道病毒感染影响疾病结局的潜在作用和分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Enteroviruses and Type 1 Diabetes: Multiple Mechanisms and Factors?

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by insulin deficiency and resultant hyperglycemia. Complex interactions of genetic and environmental factors trigger the onset of autoimmune mechanisms responsible for development of autoimmunity to β cell antigens and subsequent development of T1D. A potential role of virus infections has long been hypothesized, and growing evidence continues to implicate enteroviruses as the most probable triggering viruses. Recent studies have strengthened the association between enteroviruses and development of autoimmunity in T1D patients, potentially through persistent infections. Enterovirus infections may contribute to different stages of disease development. We review data from both human cohort studies and experimental research exploring the potential roles and molecular mechanisms by which enterovirus infections can impact disease outcome.

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来源期刊
Annual review of medicine
Annual review of medicine 医学-医学:内科
CiteScore
24.90
自引率
0.00%
发文量
58
期刊介绍: The Annual Review of Medicine, which has been published since 1950, focuses on important advancements in diverse areas of medicine. These include AIDS/HIV, cardiology, clinical pharmacology, dermatology, endocrinology/metabolism, gastroenterology, genetics, immunology, infectious disease, neurology, oncology/hematology, pediatrics, psychiatry, pulmonology, reproductive medicine, and surgery. The journal's current volume has transitioned from a gated access model to an open access model through the Annual Reviews' Subscribe to Open program. All articles published in the journal are now available under a CC BY license.
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