UC San Francisco scientists announced on Apr. 16 that they are advancing efforts to address the challenges facing people with type 1 diabetes, a disease affecting an estimated 2.1 million Americans. The UCSF Diabetes Center, celebrating its twenty-fifth anniversary this year, continues to pursue new treatments and research aimed at functional cures for the chronic condition.
Type 1 diabetes requires constant monitoring and lifelong insulin injections due to the pancreas losing its ability to produce insulin. This form of diabetes accounts for about eight to ten percent of all diabetes cases in the United States and carries a higher risk of complications such as heart disease, stroke, and blindness.
Mark Anderson, M.D., Ph.D., director of the UCSF Diabetes Center, said that advances have been made since UCSF helped discover biomarkers for type 1 diabetes in the 1980s. He explained that “the Food and Drug Administration approved the first immune therapy, Teplizumab, to delay the onset of type 1 diabetes in 2022.” Anderson described how research led by Professor Emeritus Jeffrey Bluestone identified T cells as central players in autoimmune attacks on insulin-producing cells. This work contributed directly to developing Teplizumab: “Ultimately, we were able to give the antibody drug (Teplizumab), to people who we knew were on their way to developing type 1 diabetes because they had antibody biomarkers in their blood. The antibody therapy worked and delayed the onset of type 1 diabetes by years in many patients, which led to the 2022 approval.”
The center is also involved in cellular therapy research including islet transplantation—a procedure used for severe cases—led by Surgery Professor Andrew Posselt. In clinical trials at UCSF, stem cell-derived insulin-producing cells have been transplanted into patients who then no longer need daily insulin but must take lifelong immunosuppressive drugs.
Researchers are now exploring ways around immune suppression through regulatory T cells (Tregs). Professor Qizhi Tang leads efforts alongside Audrey Parent at reprogramming Tregs so they can prevent harmful immune responses without weakening overall immunity. Anderson said this approach is promising: “The Tregs will help shut down that unwanted immune response against insulin-producing cells but leave the rest of the immune system intact.”
Anderson concluded that current work aims toward achieving antigen-specific tolerance—shutting off only those parts of immunity responsible for attacking insulin-producing cells while preserving protective functions: “We are now beginning to see the early steps toward making this a reality come together.”
