Molecular Mechanisms in the Etiology and Pathogenesis of Autoimmune Diabetes

Dear Colleagues,

Autoimmune diabetes, commonly referred to as type 1 diabetes mellitus (T1D), is a persistent immune-mediated condition marked by a lack of insulin due to the destruction of pancreatic beta cells, leading to elevated blood glucose levels. The cause of autoimmune diabetes remains unknown, but is believed to involve a combination of genetic and environmental factors. Genetic factors may play a minor role as only 15% of children with T1D have close relatives with T1D. As T1D is more abundant in developed countries (North America, Western Europe and Australia) than in developing countries, where infectious diseases are more common, it is suspected that a lack of stimulation of the immune system may increase the risk of autoimmune diseases like T1D, supporting the so-called “hygiene hypothesis”. Although the discovery of insulin in 1921 transformed T1D from an invariable fatal disease into a life-long chronic condition, people with T1D have a reduced life expectancy due to a risk of complications. Consequently, there is a great need to develop immune-based therapies and beta cell replacement strategies for its treatment.

This Special Issue aims to present readers with an up-to-date overview of ongoing molecular research addressing questions related to autoimmune diabetes physiopathology, ranging from its etiology and pathogenesis to therapeutic approaches. Both original research articles and comprehensive reviews of high educational value covering different aspects of autoimmune diabetes are welcome.

Prof. Dr. Jens Høiriis Nielsen
Guest Editor

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• type 1 diabetes
• autoimmune diabetes
• pathophysiology
• pancreatic beta cell
• immune therapies
• beta cell replacement therapy
• stem cell development