Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection.
Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection.
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DOI：
10.3390/microorganisms8091419
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发表时间：
2020-09-15
期刊：
影响因子：
4.5
通讯作者：
Morgan NG
中科院分区：
文献类型：
--
作者：
Akhbari P;Richardson SJ;Morgan NG
肠道病毒（EV）长期以来一直与1型糖尿病（T1D）的发病机制有关，越来越多的证据表明，病毒诱导的自身免疫与T1D中胰腺β细胞的损失有关。包括干扰素（IFN）在内的炎性细胞因子形成了抵抗病毒感染的主要防线，并且它们的慢性升高是许多自身免疫性疾病的标志性特征。IFN在激活和调节先天性和适应性免疫应答中起关键作用，并且为了这样做，它们调节基因和转录因子网络的表达，这些基因和转录因子一般被称为IFN刺激基因（ISG）。ISG进而调节从细胞代谢和生长调节到内质网（ER）应激和凋亡的关键细胞过程。最近的研究表明，干扰素还在表观遗传以及转录后和翻译后水平上调节基因表达。因此，IFN形成了连接T1D起始和进展中涉及的各种遗传、环境和免疫因素的关键环节。因此，更好地了解干扰素调节β细胞功能和存活的机制对于解释病毒诱导的T1 D的发病机制至关重要。这应该提供预防、减缓甚至逆转β细胞损伤的手段。
Enteroviruses (EVs) have long been implicated in the pathogenesis of type 1 diabetes (T1D), and accumulating evidence has associated virus-induced autoimmunity with the loss of pancreatic beta cells in T1D. Inflammatory cytokines including interferons (IFN) form a primary line of defence against viral infections, and their chronic elevation is a hallmark feature of many autoimmune diseases. IFNs play a key role in activating and regulating innate and adaptive immune responses, and to do so they modulate the expression of networks of genes and transcription factors known generically as IFN stimulated genes (ISGs). ISGs in turn modulate critical cellular processes ranging from cellular metabolism and growth regulation to endoplasmic reticulum (ER) stress and apoptosis. More recent studies have revealed that IFNs also modulate gene expression at an epigenetic as well as post-transcriptional and post-translational levels. As such, IFNs form a key link connecting the various genetic, environmental and immunological factors involved in the initiation and progression of T1D. Therefore, gaining an improved understanding of the mechanisms by which IFNs modulate beta cell function and survival is crucial in explaining the pathogenesis of virally-induced T1D. This should provide the means to prevent, decelerate or even reverse beta cell impairment.
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DOI：
10.1126/science.aad2791
发表时间：
2016-02-12
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Delong T;Wiles TA;Baker RL;Bradley B;Barbour G;Reisdorph R;Armstrong M;Powell RL;Reisdorph N;Kumar N;Elso CM;DeNicola M;Bottino R;Powers AC;Harlan DM;Kent SC;Mannering SI;Haskins K
通讯作者：
Haskins K
影响因子：
82.9
作者：
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--
影响因子：
--
作者：
BODANSKY, HJ;STAINES, A;CARTWRIGHT, R
通讯作者：
CARTWRIGHT, R
影响因子：
4.4
作者：
Bovin, LF;Rieneck, K;Bendtzen, K
通讯作者：
Bendtzen, K
影响因子：
37.8
作者：
Bouin, Alexis;Gretteau, Paul-Antoine;Andreoletti, Laurent
通讯作者：
Andreoletti, Laurent