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dc.contributor.authorMorgan, Noel
dc.contributor.authorRichardson, S. J.
dc.date.accessioned2021-03-23T14:51:22Z
dc.date.available2021-03-23T14:51:22Z
dc.date.issued2020-09-15
dc.identifier.citationAkhbari P, Richardson SJ, Morgan NG. Type 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infection. Microorganisms. 2020 Sep 15;8(9):1419.en_US
dc.identifier.pmid32942706
dc.identifier.doi10.3390/microorganisms8091419
dc.identifier.urihttps://rde.dspace-express.com/handle/11287/621684
dc.description.abstractEnteroviruses (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.en_US
dc.language.isoenen_US
dc.publisherMultidisciplinary Digital Publishing Institueen_US
dc.relation.urlhttps://www.mdpi.com/resolver?pii=microorganisms8091419en_US
dc.rights© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)en_US
dc.rightsCC0 1.0 Universal*
dc.rights.urihttp://creativecommons.org/publicdomain/zero/1.0/*
dc.subjectEndoplasmic Reticulum (ER) stressen_US
dc.subjectInterferon Stimulated Genes (ISG)en_US
dc.subjectapoptosisen_US
dc.subjectautoimmune diseaseen_US
dc.subjectenterovirusen_US
dc.subjectinnate immunityen_US
dc.subjectWessex Classification Subject Headings::Endocrinology::Diabetesen_US
dc.titleType 1 Diabetes: Interferons and the Aftermath of Pancreatic Beta-Cell Enteroviral Infectionen_US
dc.typeJournal Articleen_US
dc.identifier.journalMicroorganismsen_US
dc.identifier.pmcidPMC7565444
dc.description.noteThis article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.en_US
dc.description.fundingThis work was supported by a JDRF Career Development Award (5-CDA-2014-221-A-N) to S.J.R., a JDRF research grant awarded to the network of Pancreatic Organ Donors-Virus (nPOD-V) consortium (JDRF 25-2012-516), and an MRC Project Grant MR/P010695/1 awarded to S.J.R. and N.G.M.en_US
dc.type.versionPublisheden_US
dc.description.admin-notepublished version, accepted version, submitted versionen_US


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© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
Except where otherwise noted, this item's license is described as © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)