Moreover, the lab-grown cells could solve a longstanding logistical challenge in beta cell transplantation: the shortage of donor cells. Currently, a single transplant often requires beta cells from three or four donors, while most organ transplants need only a one-to-one match. The team’s engineered beta cells, by contrast, can be manufactured in the laboratory, frozen and stored for extended periods without losing quality. This could ensure a reliable, scalable source of donor material for future treatments.
The ultimate goal is to generate a complete off-the-shelf therapy, melding the engineered Tregs with the novel beta cells to create a ready-to-use treatment that can be distributed widely and administered through transplantation.
“We’re trying to develop a therapy that would work for all people with type 1 diabetes at every stage, even people who have had the disease for many years and have no beta cells left,” said Ferreira.
Measuring success and looking ahead
Getting these therapies into clinics will take time. Ferreira and his team have a number of questions and obstacles to overcome before treatments can be offered to the public. For example, one of the key questions this study aims to answer is how long the treatment remains effective. In preclinical models using humanized mice, the effects last for up to a month, the longest time assessed. The new Breakthrough T1D grant will allow the team to investigate ways to extend this window, refine delivery methods and evaluate whether combining multiple doses might yield more durable results.
By merging the disciplines of stem cell biology, gene editing and immunoregulation, Ferreira’s team is creating not just a therapy but a model for how science can reprogram the body’s natural systems to heal itself. Their work may one day mean freedom from daily insulin injections and a future where type 1 diabetes is not just managed but cured.
If successful, this work could mark a turning point in regenerative and immune-based medicine.
“I think this can change how medicine is done,” Ferreira said. “Instead of treating symptoms, we can actually replace the missing cells. By doing this work, we are likely to further understand how T1D starts, how it develops and how it can be treated.”
