Clayton Mathews, Ph.D.
Professor of Infectious Diseases and Immunology
College of Veterinary Medicine
Type 1 diabetes is often understood as a disease driven by the immune system’s destruction of insulin- producing cells. Clayton Mathews’ research has helped reshape that view by showing that the insulin-producing cells themselves play a critical role in their own survival — and failure. Mathews’ work aims to better understand how Type 1 diabetes develops at a cellular and molecular level, with the goal of identifying ways to prevent or cure the disease. His research explores not only how the immune system attacks pancreatic beta cells, but also how those cells respond to stress and defend themselves.
One of Mathews’ most influential contributions has been demonstrating that beta cells are not passive targets but active participants in the disease process. His research showed that some beta cells lack critical protective mechanisms, making them more vulnerable to immune attack. He also identified genetic differences that allow certain cells to resist destruction, providing new insights into why some individuals may be naturally protected from the disease. These findings challenged long-standing assumptions and opened new directions for research into prevention and treatment. A second major focus of his work examines the role of free radicals — highly reactive molecules involved in cellular stress — in the development of diabetes. His studies have shown how these molecules contribute to cell damage, while also revealing that they play complex signaling roles within the immune system. By identifying how these processes function, the research is helping to clarify mechanisms that drive autoimmune disease and suggesting new targets for intervention.
More recently, Mathews has advanced understanding of how beta cells fail during the early stages of disease. His work using human tissue has shown that even when cells remain present, they may lose their ability to respond to glucose, effectively becoming “blind” to signals that normally trigger insulin release. This discovery challenges existing models of disease progression and suggests that restoring cell function may be as important as preventing cell loss.