More MS news articles for Feb 2002

Antibody Reverses Experimental Diabetes Without Compromising Immune Function

Feb 2002
Reuters Health

Non-FcR-binding CD3 antibodies, currently being investigated clinically for treatment of type 1 diabetes mellitus, do not comprise the host's antiviral immune competence.

The finding comes from a study using a mouse model of virally induce autoimmune diabetes, reported in the Journal of Immunology for January 15.

Dr. Matthias G. von Herrath, of the La Jolla Institute for Allergy and Immunology in San Diego, California, and colleagues explain that in this model, type 1 diabetes develops within 2 weeks after infection with lymphocytic choriomeningitis virus (LCMV). The LCMV, which infects only beta cells, is seen by the immune system of these transgenic mice as a self-antigen and infected islet cells are destroyed by antigen-specific T cells.

The investigators treated groups of 8 to 10 LCMV-infected mice for 5 days with CD3-F(ab')-2. They found that treatment was "most effective during a clearly define prediabetic phase and prevented up to 100% of diabetes. " However, at a later phase when most beta cells are destroyed, treatment caused reversion of diabetes in 75% of the animals.

The authors note that this is the first observation of an antibody's ability to reverse established disease.

After treatment with CD3-F(ab')-2, the mice were as capable as untreated mice of clearing LCMV infection, as well as infection with Pichinde and vaccinia viruses. Dr. von Herrath and his associates suggest that "administration of CD3-F(ab')-2 appears to be a safe and effective way to prevent autoimmunity by systemically modulating the immune system to a sufficient, but not excessive degree, which is reflected in the ability to still clear viral infections."

These findings, the authors conclude, support the potential value of using non-FcR-binding antibodies to treat prediabetic subjects and in recipients of islet allografts as well as in patients with recent onset diabetes.

J Immunol 2002;168:933-941.

Reuters Health Information 2002. © 2002 Reuters Ltd