Washington, Dec 19 (ANI): An antibody used in the treatment of certain cancers and rheumatoid arthritis may be a promising treatment for diabetes, say researchers at the Yale School of Medicine.

The boffins conducted a test on mice using the antibody, rituximab (anti-CD20), which depletes B cells that have been found to play a role in autoimmune diseases by interacting with T cells of the immune system.

T cells destroy insulin-producing cells directly in the pancreas, leading to type 1 diabetes.

Li Wen, senior research scientist in the division of endocrinology, said that the study showed that once B cells were depleted, regulatory cells can emerge.

Our paper shows, for the first time, that after successful B cell depletion, regulatory cells emerge that can continue to suppress the inflammatory and autoimmune response even after the B cells return, Wen said.

Even more strikingly, we found that these regulatory cells include both B and T cells.

To find if B cell depletion might prove to be a therapy for type 1 diabetes, Wen and her colleague at Yale, Mark Shlomchik, M.D., professor of laboratory medicine and immunobiology, engineered mice predisposed to diabetes and had the human version of CD20, the molecule rituximab targets, on the surface of their B cells.

They then treated the rodents with a mouse version of rituximab to deplete B cells in them either before diabetes onset, or within days of diagnosis with diabetes.

During the course of the study the researchers noted that treatment with the drug significantly delayed diabetes onset in pre-diabetic mice by 10- to 15-weeks.

The equivalent period for humans would be approximately 10 to 15 years.

Of the 14 mice that already had diabetes, five stopped needing insulin for two to five months.

These studies suggest that B cells can have dual roles in diabetes and possibly other autoimmune diseases. The B cells might promote disease initially, but after being reconstituted following initial depletion with rituximab, they actually block further disease. This means that multiple rounds of medication to deplete the B cells might not be necessary or even advisable, Shlomchik added.

The study is published in the Journal of Clinical Investigation. (ANI)