They used a technique to label the "killer" (CD8) T cells that recognize and kill the beta cells. To explore what makes Type 1 diabetes unique, the researchers turned to a mouse model of the disease that closely mirrors what happens in people with the disease. When 80% or more of the beta cells are killed, the body can no longer regulate the level of glucose in the blood and diabetes results. Type 1 diabetes is caused when the body starts making T cells that specifically recognize and kill the insulin-producing cells of the pancreas. This type of stem-like T cell has never been seen before in autoimmune diseases, and the researchers think it could hold important lessons for improving the treatment of both autoimmune diseases and cancer. Researchers reported in the journal Nature, on November 30, 2021, that the ability of autoimmune T cells to continue fighting is dependent upon a population of stem-like T cells that perpetually resupply the stock of self-reactive T cells. Now, four years later, the results are in. Schietinger's research team, particularly Sofia Vaccarino Gearty, an MD/PhD student in the lab, and scientists Doron Betel, Friederike Dündar, and Paul Zumbo from Weill Cornell Medicine. The project became a collaborative effort between Dr. Schietinger was awarded a National Institutes of Health (NIH) Director's New Innovator Award in 2017, a funding opportunity that specifically supports high-risk, high-reward science. To pursue this ambitious research project, Dr. "We thought if we could figure out how autoimmune T cells are programmed, then we could take that information and apply it to tumor-specific T cells to make them more effective cancer killers." "This is a real mystery in the field," says Andrea Schietinger, a tumor immunologist in the Sloan Kettering Institute (SKI) at Memorial Sloan Kettering Cancer Center who studies the phenomenon of immune cell dysfunction in cancer. Why does the immune system behave so differently in the two cases? No one knows.