Most patients with Type 1 diabetes (T1D) are unable to achieve levels of long-term metabolic control sufficient to avoid long-term complications. Even with the most sophisticated insulin regimes, such as sensor augmented pump therapy, used in the setting of clinical trials, less than 30% of patients achieve target levels of glucose control and in the “real world” rates are typically less than 16%. The personal effort required to achieve these glycaemic targets is so high that compliance is poor especially amongst young people. Although advances in insulin delivery systems continue to be made, there is little indication that they will be able to match the level of metabolic control and flexibility that can be achieved by functioning pancreatic beta cells.

Preservation of beta cell function has the potential to improve metabolic control more effectively, at lower cost and with higher patient acceptability than insulin replacement therapy.

The EE-ASI consortium therefore propose that biological therapies which preserve beta cell function by building on current immunological therapy approaches represent the optimal method of improving glycaemic control, quality of life and long-term outcomes in recently diagnosed Type 1 diabetes.

Type 1 Diabetes (T1D) in few words…
T1D is one of the most common severe chronic autoimmune diseases (AIDs) worldwide. In Europe its incidence is rapidly rising in children, with a predicted 70% increase in cases over the next 15 years. In addition the age at diagnosis is decreasing, with a predicted doubling of cases in children under the age of 5 years in the same period. The aetiology (cause) of T1D is the autoimmune-mediated progressive destruction of insulin-producing pancreatic beta cells leading to insulin deficiency resulting in hyperglycaemia at clinical diagnosis.

Why immunotherapies in the context of T1D?

An effective immunological therapy would preserve remaining beta cell function in patients treated at the time of diagnosis of T1D but also have application in individuals with long-standing diabetes by use in combination with restorative and regenerative approaches, protecting new or regenerating beta cells from destruction by the immune system, currently a key bottleneck. Furthermore, such a therapeutic could also be used in “pre-diabetes” to prevent the development of clinical diabetes in individuals identified by autoantibody screening to be at high risk.