Researchers Report Finding Potential Multiple Sclerosis 'Off Switch'

September 9, 2014

When autoimmune diseases like multiple sclerosis attack a patient's body from the inside it can be a difficult reminder of how hard it can be to treat a condition from the inside out.

When autoimmune diseases like multiple sclerosis attack a patient’s body from the inside it can be a difficult reminder of how hard it can be to treat a condition from the inside out.

Recently, a team from the University of Bristol announced it had found a way to ‘switch off’ aspects of the body’s autoimmune response so that rather than causing harm to the body these cells protect it. The results of this study were published in Nature Communications and researchers are hopeful they could lead to the development of antigen-specific immunotherapies not only for patients with MS but other conditions like Graves’ disease, type 1 diabetes, and lupus.

A statement from the school said the researchers targeted the cells that cause autoimmune disease to convert them from offensive to defensive in a process similar to “allergic desensitization,” which is already used in treating patients with allergies.

“The Bristol group has now revealed how the administration of fragments of the proteins that are normally the target for attack leads to correction of the autoimmune response,” the statement noted.

“Most importantly, their work reveals that effective treatment is achieved by gradually increasing the dose of antigenic fragment injected,”

Another advantage to this form of therapy, the statement said, is that by only working with certain cells there is no need for “immune suppressive drugs,” which can bring severe side effects along with their benefits.

Lead researcher, Professor David Wraith said, “Insight into the molecular basis of antigen specific immunotherapy opens up exciting new opportunities to enhance the selectivity of the approach while providing valuable markers with which to measure effective treatment.”

The research team included representatives from Bristol University’s School of Cellular and Molecular Medicine and the Department of Computer Science. Following the study clinical development procedures were undertaken by Apitope, which is a spin-out of the school. Funding was provided by the Wellcome Trust.