A new study published in Cell Reports revealed that there is a possibility that new medications could block the immune system from destroying beta cells and prevent type 1 diabetes from developing in at-risk or early-onset patients. The study suggested that the causes of type 1 diabetes focus more on the autoimmune response, where the immune system destroys pancreatic islet beta cells which help to produce insulin in the body. 

In the study, the researchers tested several drugs that inhibit the 12/15-Lipoxygenase enzyme on human beta cells. They saw that the drug, called ML355, increases levels of PD-L1, suggesting that it could interrupt the autoimmune response and prevent diabetes from developing.

Meanwhile, in 2012, Sarah Tersey, Ph.D., Research Associate Professor at UChicago hypothesized that the beta-cell might be a central player in the development of type 1 diabetes. Dr. Jerry Nadler, MD, Dean of the School of Medicine and Professor of Medicine and Pharmacology at New York Medical College discovered the role of the 12/15-Lipoxygenase enzyme that is involved in the inflammation process of beta cells. Meanwhile, in the study, they saw that deleting Alox15 in the mice model using a drug called tamoxifen preserved beta cell destruction, followed by a reduction in infiltration of T cells in the beta-cell environment and decreased the risk of progression to type 1 diabetes.

Dr. Maureen Gannon, Ph.D., Professor of Medicine, Cell and Developmental Biology, and Molecular Physiology and Biophysics at Vanderbilt University, provided a strain of mice that was used in the study, which allowed for the knockout of the Alox15 gene. 

(Source: https://www.hindustantimes.com/lifestyle/health/type-1-diabetes-can-be-prevented-if-focus-on-beta-cells-instead-of-immune-system-says-study-101656475888519.html )