"These exciting results provide enormous hope that we can preserve residual beta cell function by modulating the autoimmune attack and in fact change the clinical course of type 1 diabetes," said JDRF executive vice president for research Richard Insel.
"There is no other current treatment that can actually change the clinical course once the disease has begun. This study shows we are on the right track, and opens the door for researchers to target this treatment specifically to individuals who would receive the most benefit," he added.
The Juvenile Diabetes Research Foundation (JDRF), funded much of the work of the European researchers and involved 80 newly diagnosed patients in a phase II clinical trial. The team found that patients who received the antibody over the course of six days immediately following diagnosis continued to produce their own insulin and needed less supplemental insulin to maintain normal blood glucose levels, as compared with patients who received a placebo.
This benefit was apparent at 6, 12 and 18 months after the treatment, suggesting that the protective effect is lasting - although for how long is not yet known. Moreover, side effects were minor and short-lived including flu and mono-like symptoms.
Anti-CD3 antibodies such as ChAglyCD3 and hOKT3g1 (ala-ala) are engineered to block the function of CD3 cells, immune T cells that orchestrate the destruction of islets. The antibodies prevent "activation" of the T cells after they have identified their target, disarming them once they are poised to attack.
The ChAglyCD3 drug that was used in the European study is a humanised, non-mitogenic anti-CD3 antibody, a new type of agent showing promise for this kind of intervention.
The European study takes a previous study a step further by extending the sample size and taking into account the extent of beta cell function each patient had at the beginning of treatment.
This allowed the researchers to track and compare anti-CD3 antibody's (ChAglyCD3) effect on patients who had high and low residual beta cell function initially to see how well the drug worked with patients in both categories.
The research team observed that the anti-CD3's protective effect was more pronounced in patients who had higher beta cell function at the time they received the drug.
Interventions that can preserve endogenous insulin production are expected to result in better metabolic control of diabetes, and thus delay, or reduce the risk of diabetes-related complications such as eye, nerve and kidney disease.
"We can now inform patients that a step has been made towards stopping the disease but we will also have to explain why more work is needed before a treatment will be routinely available for clinical practice," said Daniel Pipeleers, director at the JDRF Centre for Beta Cell Therapy in Europe.
The Phase II clinical trial involved 80 newly diagnosed patients, was conducted in collaboration with a team of clinicians and researchers from France, Belgium, Germany and England and is to appear in the June 23 issue of New England Journal of Medicine.
Type 1 diabetes occurs when the body's own immune cells mistakenly attack and destroy insulin-secreting beta cells in the pancreas. As long as the pancreatic beta cells can compensate for the degree of insulin resistance, glucose tolerance remains normal.
Insulin resistance and impaired beta-cell function are widely recognised as features of diabetes. It has been debated whether insulin resistance, beta-cell dysfunction, or both constitute the primary abnormality in type 2 diabetes and whether one defect precedes the other in the natural history of the disease.
According to Goldman Sachs, Diabetes is forecast by the International Diabetes Federation to increase by around 62 per cent by 2025, affecting 60-140 million people, and with a forecast prevalence to increase to 9.1 per cent and 9.7 per cent in Europe and the US over that period, the incidence of diabetic nephropathy, which occurs in 20-50 per cent of type 1 and 2 diabetic patients, is also likely to increase significantly.