Short-term treatment with a new monoclonal antibody appears to preserve residual insulin production in patients with recent onset of Type 1 Diabetes, European investigators report.

Type 1 Diabetes occurs when an autoimmune reaction knocks out insulin-producing beta cells. The newly created antibody targets a molecule called CD3 on the surface of the immune cells involved in the faulty attack on beta cells.

Experiments with mice that develop diabetes have shown that short-term treatment with anti-CD3 antibodies leads to long-term remission of the disease, Dr. Bart Keymeulen, from Brussels Free University-VUB in Belgium and his associates note in this week’s New England Journal of Medicine.

To investigate a similar strategy in humans, the researchers conducted a trial with 80 type 1 diabetic patients, ages 12 to 39 years, who had been treated for less than 4 weeks with insulin and who had symptoms for less than 6 months.

In random fashion, 40 patients were assigned to get an intravenous infusion of the anti-CD3 antibody daily for 6 days, while the remaining patients received placebo.

The average insulin dose the participants required to keep their blood sugar under control was 12 percent lower in the active treatment group after 18 months compared with the start of the study, while in the placebo group it rose 50 percent.

The antibody treatment was most effective at maintaining beta-cell function among the 16 patients who started with higher-than-average residual insulin production.

The antibodies did produce flu-like symptoms during treatment in some participants, and a mononucleosis-like syndrome after treatment stopped.

“If CD3 monoclonal antibodies are shown to be safe, perhaps their use ... could lead to improved therapies for type 1 diabetes,” Dr. Ake Lernmark, from the University of Washington in Seattle, comments in an accompanying editorial.

SOURCE: New England Journal of Medicine, June 23, 2005.