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A study has demonstrated that transplanting human embryonic stem cell–derived, insulin-producing cells shielded in capsules made with an optimized biomaterial can achieve long-term cure of diabetes in mice without the need for any immunosuppression.

Type 1 diabetes affects more than 30 million people worldwide. The disease results from the destruction of insulin-producing beta cells by an overactive immune system. Currently, individuals with diabetes are treated mainly with insulin injections that do not perfectly simulate insulin secretion from beta cells. Consequently, the person’s blood glucose levels fluctuate, despite close monitoring and frequent adjustments to insulin doses. Chronic hyperglycemia leads to irreversible tissue and organ damage, and hypoglycemia can be acutely life threatening.

Replacing lost beta cells through islet transplantation can achieve tight blood glucose control so that people with diabetes do not have to worry about their blood glucose. Currently, two major barriers limit the use of this therapy. Islets for transplantation come from the pancreases of deceased donors. However, each year, an average of 30,000 people in the US are diagnosed with type 1 diabetes, whereas an average of only 1,000 pancreases are donated for transplantation. In addition, transplant recipients have to take immunosuppressive drugs for the rest of their lives to prevent their bodies from rejecting foreign cells. Immunosuppressive drugs not only increase their risk of developing infections and malignancies, but the drugs themselves are often toxic and cause organ damage. Therefore, to realize the therapeutic potential of islet transplantation, we must have a vast source of beta cells and a drug-free approach to prevent rejection.

In this issue of Nature Medicine1, and recently in Nature Biotechnology2, Vegas et al.1, 2 showed that generating insulin-producing cells from renewable stem cells and then placing them in an immune-protective capsule before transplantation leads to an immediate and sustained correction of diabetes in mice without the need for immunosuppression (Fig. 1). This exciting advance renews our hope that, one day, this approach could enable wider application of beta cell–replacement therapy in humans.

full text: http://www.nature.com/nm/journal/v22/n3/full/nm.4060.html