Immune and cell therapy in type 1 diabetes: too little too late?

Type 1 diabetes is caused by autoimmune destruction of insulin-producing β-cells. Intensive insulin therapy protects most patients against chronic complications of diabetes, but exposes patients to acute complications like hypoglycaemia and impacts on quality of life. Therapies that aim at protecting or restoring endogenous insulin secretion might help in decreasing the risk of severe hypoglycemia and long-term complications.

This article reviews the literature of clinical immunotherapy and β-cell transplantation in treatment of type 1 diabetes with specific focus on the effect on preserving and restoring β-cell mass.

Several studies in recent-onset type 1 diabetic patients have provided proof of principle that immunotherapy can preserve residual functional β-cell mass. The observation that this strategy is most effective early in the disease process opens possibilities of arresting and even preventing type 1 diabetes. In patients with too few or no surviving β-cells, current protocols of β-cell transplantation can restore functional β-cell mass up to 25% of levels in healthy controls. Unfortunately, both strategies to date are followed by progressive decline of endogenous insulin secretion later on. Strategies to restore functional β-cell mass to a higher level and to restore immune tolerance are thus needed.