Can a protein prevent the destruction of insulin-producing cells in autoimmune diabetes?
Type 1 diabetes is an autoimmune disease that generally develops in young patients. The disease is characterised by insulin deficiency. How the insulin-secreting cells in the pancreas (known as β-cells) are lost in type 1 diabetes is a question that remains to be answered. Different candidate genes related to the pathogenesis of type 1 diabetes have been postulated by scanning the entire genome of patients looking for common genetic variation. The role of those candidate proteins and the mechanisms of β-cell dysfunction during the transition from inflammation to diabetes is one of the key unanswered questions in our research field.
In the recent publication in the journal Diabetes from the Signal Transduction and Metabolism Laboratory, we discovered a new molecular mechanism whereby a type 1 diabetes candidate protein PTPN2 provides protection to β-cells in pre-clinical models of autoimmune diabetes. The deficiency of PTPN2 in the β-cells results in endoplasmic reticulum failure and exacerbated inflammatory response. We used mouse models, stem and primary human cells and cell lines to clarify the mechanism of PTPN2 action as anti-inflammatory protein. Our work highlights the potential utility of targeted pharmacological approaches to improve β-cell defences in combating the development of autoimmune diabetes.
The first authors of the article are Bernat Elvira (FNRS CR) and Valerie Vandenbempt (FNRS Aspirant) in collaboration with laboratories from Belgium, Finland, Australia and the Netherlands. The senior author is Esteban Gurzov Welbio investigator and head of the Signal Transduction and Metabolism Laboratory. Credit to Eduardo Gilglioni for drawing the cartoon.
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