Signature for Beta-Cell Autoimmunity Predicts Type 1 Diabetes

Therefore, there is a clear and urgent need for new biomarkers that predict the onset of the autoimmune reaction preceding autoantibody positivity or reflect progressive beta-cell destruction.

A team of scientists working with the University of Turku (Turku, Finland) used mRNA-sequencing-based analysis of 306 samples including fractionated samples of CD4+ and CD8+ T cells as well as CD4-CD8- cells fractions and unfractionated peripheral blood mononuclear cell (PBMC) samples longitudinally collected from seven children that developed beta-cell autoimmunity (Cases) at a young age and their matched controls.

The investigators identified transcripts, including interleukin-32 (IL32) that were upregulated before T1D-associated autoantibodies appeared. Single-cell RNA-seq studies revealed that high IL32 in Case samples were contributed mainly by activated T cells and NK cells. Further, they showed that IL32 expression can be induced by a virus and cytokines in pancreatic islets and beta-cells, respectively.

The authors concluded that their results provide a basis for early detection of aberrations in the immune system function before T1D and suggest a potential role for IL32 in the pathogenesis of T1D. Riitta Lahesmaa, MD, a Professor of Biotechnology and senior author of the study, said, “Our results provide a starting point for identifying those children who are likely to develop type 1 diabetes later. Next, we will validate and expand the study in a larger cohort and analyze the role of the signature molecules in the pathogenesis of type 1 diabetes. Our goal is to develop tools and means that would enable the prevention of type 1 diabetes.” The study was published in the July 2019 issue of the journal Diabetes.

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