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Development of type 1 diabetes varies between children, new study finds

Published on 28.11.2023
Tampere University
Microscope image of pancreatic islet cells showing red, green and blue.
The figure shows enterovirus-infected pancreatic islet cells. Glucagone, a hormone that regulates the metabolism of carbohydrates, is shown in red, insulin in cyan and enterovirus in green. Enteroviruses can be seen in insulin positive beta cells. Image by Pia Leete, University of Exeter Medical School, Sarah Richardson, University of Exeter Medical School and Jutta Laiho, Tampere University
A new study highlights the role of pancreatic islet autoantibodies in the different disease mechanisms leading to type 1 diabetes. Changes in gene expression were detected already a year before the islet autoantibodies appeared. The results also support the role of enteroviruses in the development of the disease.

Together with international partners, researchers at Tampere University investigated the mechanisms that contribute to the development of type 1 diabetes, where the body’s own immune system attacks the insulin producing cells in the pancreas, which are essential for balancing blood glucose levels. Genetic and environmental factors increase the risk, and, for example, enteroviral infections have previously been associated with type 1 diabetes.

“According to the current view, enteroviruses can enter the pancreas where they cause a chronic infection. This leads to the destruction of immune producing cells in genetically susceptible individuals. Type 1 diabetes is more common in Finland than anywhere else in the world, although its prevalence has also rapidly increased in other developed countries,” Professor Heikki Hyöty comments.

The newly published study is part of the Environmental Determinants of Diabetes in the Young (TEDDY) -project, where over 8,000 genetically susceptible children were followed up from birth until they turned 15. The study was conducted in four countries: Finland, Germany, Sweden, and United States.

During the follow-up, the children gave regular samples that enabled the detection of viral infections as well as gene expression and cell types that contribute to the functions of the immune system. In gene expression, cells produce molecules that are encoded by the genome. This study focused on genes expressed by white blood cells.

Significant changes in gene expression as well as immune cell type proportions were observed already 9–12 months before the first appearance of pancreatic islet autoantibodies, which often marks the beginning of the autoimmune process that precedes type 1 diabetes onset. In the study, children were grouped by the first appearing autoantibody and the detected differences between the groups further support the notion that the development of the disease varies between children.

Furthermore, a robust immune response to the enterovirus was detected in the children who did not develop islet autoantibodies later, whereas the immune response varied in children that later went on to develop autoantibodies, suggesting that enteroviruses may not be completely eradicated in some children, but can linger in the body. This supports the view that enteroviruses play a role in the onset of the disease.

“These results help us to understand the disease mechanisms and they further highlight the part enterovirus plays in the process. This brings us closer to the goal of earlier diagnosis and treatment,” Professor Matti Nykter added.

The study, recently published in Nature Communications, was conducted by Matti Nykter’s, Heikki Hyöty’s and Kirsi Rautajoki’s research groups at Tampere University. The investigation to further elucidate the mechanisms that lead to type 1 diabetes continues in several EU-funded international studies.

Publication information:

Lin, J., Moradi, E., Salenius, K. et al. Distinct transcriptomic profiles in children prior to the appearance of type 1 diabetes-linked islet autoantibodies and following enterovirus infection. Nat Commun 14, 7630 (2023). Read the article online.

Further information

Heikki Hyöty
heikki.hyoty [at]

Kirsi Rautajoki
kirsi.rautajoki [at]

Matti Nykter
matti.nykter [at]