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dc.contributor.authorRichardson, SJ
dc.contributor.authorMorgan, N
dc.date.accessioned2018-07-17T13:14:23Z
dc.date.issued2018-07-29
dc.description.abstractThe development of islet autoimmunity and type 1 diabetes has long been linked with enteroviral infection but a causal relationship has proven hard to establish. This is partly because much of the epidemiological evidence derives from studies of neutralising antibody generation in blood samples while much less attention has been paid to the pancreatic beta cells as a site of infection. Nevertheless, recent studies have revealed that beta cells express specific enteroviral receptors and that they can sustain a productive enteroviral infection. Importantly, they can also mount antiviral responses which attenuate viral replication and may favour the establishment of a persistent enteroviral infection. Together, these responses combine to create the Trojan horse by which enteroviruses might precipitate islet autoimmunityen_GB
dc.description.sponsorshipWe are pleased to acknowledge financial support via a JDRF Career Development Award (5-CDA2014-221-A-N) to SJR, an MRC Project Grant (MR/P010695/1) to SJR & NGM and project grants from Diabetes UK (15/0005156 & 16/0005480) to NGM & SJRen_GB
dc.identifier.citationVol. 43, pp. 11-19.en_GB
dc.identifier.doi10.1016/j.coph.2018.07.006
dc.identifier.urihttp://hdl.handle.net/10871/33467
dc.language.isoenen_GB
dc.publisherElsevieren_GB
dc.rights© 2018 The Authors. Open Access funded by Medical Research Council. Under a Creative Commons license (http://creativecommons.org/licenses/by/4.0/).
dc.titleEnteroviral infections in the pathogenesis of type 1 diabetes: new insights for therapeutic interventionen_GB
dc.typeArticleen_GB
dc.identifier.issn1471-4973
dc.descriptionThis is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record.en_GB
dc.identifier.journalCurrent Opinion in Pharmacologyen_GB


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