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dc.contributor.authorWyatt, R. C.
dc.contributor.authorRichardson, S. J.
dc.date.accessioned2020-11-09T10:42:16Z
dc.date.available2020-11-09T10:42:16Z
dc.date.issued2019-12-09
dc.identifier.citationWyatt RC et al. What the HLA-I!-Classical and Non-classical HLA Class I and Their Potential Roles in Type 1 Diabetes. Curr Diab Rep. 2019 Dec 9;19(12):159.en_US
dc.identifier.pmid31820163
dc.identifier.doi10.1007/s11892-019-1245-z
dc.identifier.urihttps://rde.dspace-express.com/handle/11287/621533
dc.description.abstractPurpose of review: Hyperexpression of classical HLA class I (HLA-I) molecules in insulin-containing islets has become a widely accepted hallmark of type 1 diabetes pathology. In comparison, relatively little is known about the expression, function and role of non-classical subtypes of HLA-I. This review focuses on the current understanding of the non-classical HLA-I subtypes: HLA-E, HLA-F and HLA-G, within and outside the field of type 1 diabetes, and considers the possible impacts of these molecules on disease etiology. Recent findings: Evidence is growing to suggest that non-classical HLA-I proteins are upregulated, both at the RNA and protein levels in the pancreas of individuals with recent-onset type 1 diabetes. Moreover, associations between non-classical HLA-I genotypes and age at onset of type 1 diabetes have been reported in some studies. As with classical HLA-I, it is likely that hyperexpression of non-classical HLA-I is driven by the release of diffusible interferons by stressed β cells (potentially driven by viral infection) and exacerbated by release of cytokines from infiltrating immune cells. Non-classical HLA-I proteins predominantly (but not exclusively) transduce negative signals to immune cells infiltrating at the site of injury/inflammation. We propose a model in which the islet endocrine cells, through expression of non-classical HLA-I are fighting back against the infiltrating immune cells. By inhibiting the activity and function on NK, B and select T cells, the non-classical HLA-I, proteins will reduce the non-specific bystander effects of inflammation, while at the same time still allowing the targeted destruction of β cells by specific islet-reactive CD8+ T cells.en_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.urlhttps://dx.doi.org/10.1007/s11892-019-1245-zen_US
dc.rightsOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.en_US
dc.rightsCC0 1.0 Universal*
dc.rights.urihttp://creativecommons.org/publicdomain/zero/1.0/*
dc.subjectHLA-Een_US
dc.subjectHLA-Fen_US
dc.subjectHLA-Gen_US
dc.subjectHLA-Ien_US
dc.subjectImmune systemen_US
dc.subjectNon-classical HLA-Ien_US
dc.subjectType 1 diabetesen_US
dc.subjectWessex Classification Subject Headings::Endocrinology::Diabetesen_US
dc.titleWhat the HLA-I!-Classical and Non-classical HLA Class I and Their Potential Roles in Type 1 Diabetesen_US
dc.typeJournal Articleen_US
dc.identifier.journalCurrent Diabetes Reportsen_US
dc.identifier.pmcidPMC6901423
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.fundingWe are pleased to acknowledge financial support via a JDRF Career Development Award (5-CDA-2014-221-A-N), a JDRF Strategic Research Agreement (JDRF 2-SRA-2018-474-S-B), an MRC Project Grant (MR/P010695/1) and project grants from Diabetes UK (15/0005156 & 16/0005480) to SJR. GL was supported by the Diabetes Research Institute Foundation. IG has a project grant from National Institute of Health (UC4 DK104155).en_US
dc.type.versionPublisheden_US
dc.description.admin-notepublished version, accepted version (12 month embargo)en_US


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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
Except where otherwise noted, this item's license is described as Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.