Scientists discovered a way to potentially reverse autoimmune diseases.
Researchers uncovered how cells convert from being aggressive to protecting against disease, the University of Bristol reported. The team hopes the new insight will open the door for antigen-specific immunotherapy to be used as treatment for a number of autoimmune disorders such as "multiple sclerosis (MS), type 1 diabetes, Graves' disease and systemic lupus erythematosus (SLE)."
The scientists successfully targeted the cells responsible for autoimmune disease by reducing their aggression towards the body's own tissue while converting them into those able to fight disease.
In order to figure out this method the researchers looked inside immune cells to see which genes and proteins were switched on and off by treatment. They found changes in gene expression could help explain how effective treatments lead to the conversion of aggression in cells. The desired outcome occurs when the body's immune system leaves its own tissue alone while still protecting against infection.
The researchers were able to accomplish this by targeting faulty cells, allowing treatment without the need for immune suppressive drugs associated with harsh side effects. These side effects can include: "infections, development of [tumors] and disruption of natural regulatory mechanisms," the University of Bristol reported.
"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. These findings have important implications for the many patients suffering from autoimmune conditions that are currently difficult to treat," said Professor David Wraith, who led the research."
The new treatment could improve the quality of life for millions of people across the globe. It is currently in the process of clinical development through biotechnology company Apitope. The study was funded by the Wellcome Trust and was published today Sept. 3 in Nature Communications.
