A gene pathway linked to a deadly form of leukemia can offer a new way for treating autoimmune diseases, including multiple sclerosis, as per scientists at the Johns Hopkins Kimmel Cancer Center.

During the study comprising of tests in cell cultures and mice, it was found that pathway blocking via FLT3 (blood cell growth gene) interference can help in targeting an immune system cell often ignored in favor of T-cell targets in standard therapies.

From News-Medical.Net:

A characteristic of autoimmune diseases is that patients’ immune T-cells mistake normal cells in the body for foreign ones. Current therapies, such as steroids, are designed to suppress T-cell responses. But the Hopkins investigators believe that targeting dendritic cells may stop the faulty immune response at a higher “upstream” level since T-cells frequently receive their information from dendritic cells.

Testing their idea, Small and his Hopkins colleague Katherine Whartenby used an experimental compound called CEP-701, already known to block actions of the growth-promoting FLT3 gene, on human dendritic cells and in mice engineered to mimic multiple sclerosis, a disease that causes T-cells to destroy the myelin protein sheath around nerves in the central nervous system. The drug had a similar effect on dendritic cells, causing most of them to die. In the mouse model, investigators found that more of the myelin sheath was preserved in mice treated with CEP-701 than those not treated.

Donald Small, M.D., Ph.D., professor at the Johns Hopkins Kimmel Cancer Center, whose findings appear in the Proceedings of the National Academy of Sciences, said that dendritic cells can be stopped from triggering harmful responses against a patient’s own body by using a drug to block FLT3 gene signaling.