A recent study has found that an anti-inflammation protein molecule interkeukin-27 (IL-27) prevents multiple sclerosis (MS) like diseases.
The study at Jefferson Medical College of Thomas Jefferson University and the Jefferson Hospital for Neuroscience in Philadelphia has claimed that the immune system messenger molecule may be an effective tool against MS as it blocks the onset or reverses systems in animals with MS-like diseases.
The research involved an animal model of MS called experimental autoimmune encephalomyelitis (EAE) for investigation.
The study shows the possibility that IL-27 may someday be part of a therapy to temper over-active immune responses, which are thought to be at the heart of MS, an autoimmune disease (in which the body attacks its own tissue) affecting the central nervous system.
The authors said that one of the most common neurological diseases affecting young adults is the myelin coating of nerve fibers which becomes inflamed and scarred. As a result, "messages" could not be sent through the nervous system.
As a result of which the authors tried to find the mechanism how immune response damaged the myelin sheath and axons in the brain. They had earlier observed that a signaling molecule called a cytokine, could suppress IL-17, another cytokine, and inflammation. They also knew that in other MS models, mice that lacked receptors for IL-27 developed excessive inflammation.
While the researchers gave IL-27 to the experimental mice, it showed suppressed active diseases. They witnessed similar effects from IL-27 in cultured cells that were transferred into "naïve" animals, which then produced significantly milder disease. At the same time, they also showed that IL-27 enhanced the production of IL-10, a crucial anti-inflammatory cytokine.
"We previously showed that IL-27 could suppress IL-17, here we also show that IL-27 can enhance the production of IL-10. These may both be different and complementary mechanisms by which IL-27 can suppress EAE," said Abdolmohamad Rostami, M.D., Ph.D., professor and chair of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University and the Jefferson Hospital for Neuroscience in Philadelphia.
"This is the first time that we have direct evidence that by actively giving IL-27 like a drug, we can suppress EAE in mice," he added.
Explaining that after an MS flare-up, patients recovered from the disease he said "We think that one of the ways that recovery from a disease flare-up occurs is that part of the immune system is shut off, suppressing the immune response in the brain. IL-27 appears to be crucial in this process."
Bringing to light that the team was intreseted to study 'MS Patients'and determines if similar processes were at work, Mr Rostami said "If we get similar findings in human disease, then perhaps IL-27 could be used therapeutically as a compound to suppress inflammation in the brains of MS patients."
The study first appeared in an online advance publication followed by the Nature Immunology journal on November 11, 2007.