UC San Francisco scientists mark advances in type 1 diabetes prevention and treatment

James B. Milliken, President
James B. Milliken, President
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UC San Francisco scientists announced on Apr. 16 new developments in the prevention and treatment of type 1 diabetes, building on nearly four decades of research. The UCSF Diabetes Center is marking its twenty-fifth anniversary this year, with ongoing efforts to address challenges facing patients and move closer to functional cures for the disease.

Type 1 diabetes affects an estimated 2.1 million Americans and requires lifelong management through blood monitoring or electronic devices. The disease increases the risk of complications such as heart disease, stroke, and blindness.

Mark Anderson, M.D., Ph.D., director of the UCSF Diabetes Center, said that “the center marks a quarter century of science aimed at saving lives and revolutionizing what the world thought possible in diabetes prevention and care.” He explained that type 1 diabetes is an autoimmune condition where the immune system attacks insulin-producing cells in the pancreas, leading to high blood sugar levels.

Anderson said that “the Food and Drug Administration approved the first immune therapy, Teplizumab, to delay the onset of type 1 diabetes in 2022.” This approval followed decades of research at UCSF identifying malfunctioning antibodies as biomarkers for early diagnosis. Research led by immunologist Jeffrey Bluestone helped develop Teplizumab by targeting T cells involved in attacking pancreatic cells.

The center is also advancing cellular therapies such as islet transplantation for severe cases. Anderson described clinical trials where lab-grown insulin-producing cells were transplanted into patients: “Participants are able to get off insulin, which is great. But they have to take lifelong medication to suppress their immune system…this risk makes the approach impractical for most patients.” To address this challenge, researchers like Qizhi Tang are working on using regulatory T cells (Tregs) to prevent harmful immune responses without suppressing overall immunity.

“This approach is thrilling because it is specific in nature: The Tregs will help shut down that unwanted immune response against insulin-producing cells but leave the rest of the immune system intact,” Anderson said.

Looking ahead, Anderson sees promise in developing antigen-specific tolerance—shutting off only parts of the immune system responsible for attacking insulin-producing cells while preserving normal function. “We are now beginning to see the early steps toward making this a reality come together,” he said.



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