Journal
SCIENCE ADVANCES
Volume 7, Issue 9, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.abd6527
Keywords
-
Categories
Funding
- JDRF [3-SRA-2017-492-A-N, 5-SRA-2018-557-Q-R]
- Leona M. and Harry B. Helmsley Charitable Trust [2018PG-T1D053]
- MRC [MR/P010695/1] Funding Source: UKRI
Ask authors/readers for more resources
The study reveals the presence of IFN response markers in the islets of T1D patients, which may lead to inflammation and impair beta cell function. Therapeutic interventions targeting the elimination of persistent infections and reduction of inflammation are crucial for individuals with T1D.
Previous results indicate the presence of an interferon (IFN) signature in type 1 diabetes (T1D), capable of inducing chronic inflammation and compromising beta cell function. Here, we determined the expression of the IFN response markers MxA, PKR, and HLA-I in the islets of autoantibody-positive and T1D donors. We found that these markers can be coexpressed in the same islet, are more abundant in insulin-containing islets, are highly expressed in islets with insulitis, and their expression levels are correlated with the presence of the enteroviral protein VP1. The expression of these markers was associated with down-regulation of multiple genes in the insulin secretion pathway. The coexistence of an IFN response and a microbial stress response is likely to prime islets for immune destruction. This study highlights the importance of therapeutic interventions aimed at eliminating potentially persistent infections and diminishing inflammation in individuals with T1D.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available