Journal
CURRENT OPINION IN PHARMACOLOGY
Volume 43, Issue -, Pages 11-19Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2018.07.006
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Funding
- JDRF Career Development Award [5-CDA-2014-221-A-N]
- MRC Project Grant [MR/P010695/1]
- Diabetes UK [15/0005156, 16/0005480]
- MRC [MR/P010695/1] Funding Source: UKRI
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The 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 less attention has been paid to the pancreatic beta cell 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 autoimmunity.
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