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Expression of Interferon-Stimulated Genes in Insulitic Pancreatic Islets of Patients Recently Diagnosed With Type 1 Diabetes
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Oslo Univ Hosp, Div Paediat & Adolescent Med, Oslo, Norway.;Univ Oslo, Fac Med, Oslo, Norway..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
Oslo Univ Hosp, Div Paediat & Adolescent Med, Oslo, Norway.;Univ Oslo, Fac Med, Oslo, Norway..
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2016 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 65, no 10, p. 3104-3110Article in journal (Refereed) Published
Abstract [en]

A primary insult to the pancreatic islets of Langerhans, leading to the activation of innate immunity, has been suggested as an important step in the inflammatory process in type 1 diabetes (T1D). The aim of this study was to examine whether interferon (IFN)-stimulated genes (ISGs) are overexpressed in human T1D islets affected with insulitis. By using laser capture microdissection and a quantitative PCR array, 23 of 84 examined ISGs were found to be overexpressed by at least fivefold in insulitic islets from living patients with recent-onset T1D, participating in the Diabetes Virus Detection (DiViD) study, compared with islets from organ donors without diabetes. Most of the overexpressed ISGs, including GBP1, TLR3, OAS1, EIF2AK2, HLA-E, IFI6, and STAT1, showed higher expression in the islet core compared with the peri-islet area containing the surrounding immune cells. In contrast, the T-cell attractant chemokine CXCL10 showed an almost 10-fold higher expression in the peri-islet area than in the islet, possibly partly explaining the localization of T cells mainly to this region. In conclusion, insulitic islets from recent-onset T1D subjects show overexpression of ISGs, with an expression pattern similar to that seen in islets infected with virus or exposed to IFN-gamma/interleukin-1 beta or IFN-alpha.

Place, publisher, year, edition, pages
2016. Vol. 65, no 10, p. 3104-3110
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:uu:diva-311223DOI: 10.2337/db16-0616ISI: 000388372900029PubMedID: 27422384OAI: oai:DiVA.org:uu-311223DiVA: diva2:1059592
Funder
Novo NordiskSwedish Research Council, K2011-65X-12219-15-6, K2015-54X-12219-19-4Åke Wiberg FoundationSwedish Diabetes AssociationSwedish Child Diabetes FoundationEXODIAB - Excellence of Diabetes Research in Sweden
Available from: 2016-12-22 Created: 2016-12-22 Last updated: 2017-11-29Bibliographically approved

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