期刊
DIABETES
卷 65, 期 10, 页码 3104-3110出版社
AMER DIABETES ASSOC
DOI: 10.2337/db16-0616
关键词
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资金
- South-Eastern Norway Regional Health Authority
- Novo Nordisk Foundation
- Persistent Virus Infection in Diabetes Network (PEVNET) Study Group - European Union Seventh Framework Programme [261441 PEVNET]
- Swedish Medical Research Council [VR K2011-65X-12219-15-6, K2015-54X-12219-19-4]
- Diabetes Wellness Foundation
- Stiftelsen Family Ernfors Foundation
- Ake Wiberg Foundation
- Tore Nilsson Foundation
- Swedish Diabetes Association
- Gillbergska Stiftelsen
- Barndiabetesfonden
- Beredningshandbok forskningsinfrastruktur (RFI)/Vetenskapsradet (VR) Swedish National Infrastructure for Large-Scale Sequencing and Science for Life Laboratory (SNISS), Uppsala, Sweden
- Swedish National Strategic Research Initiative EXODIAB (Excellence Of Diabetes Research in Sweden)
- JDRF
- Novo Nordisk Fonden [NNF14OC0010935, NNF16OC0021334] Funding Source: researchfish
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.
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