JCI paper shows that the therapeutic’s effects are due in part to increasing the secretion of IL-27.
Researchers at the University of California at Los Angeles found a pathway by which IFN-beta reduces disease in a mouse model of multiple sclerosis (MS), known as experimental autoimmune encephalomyelitis (EAE).
Although the drug IFN-beta is commonly used to treat individuals with relapsing-remitting MS, little is known about how it acts. In addition to being a drug, IFN-beta is produced naturally by the body during certain immune responses.
In the study, mice lacking a component of the molecule to which IFN-beta binds were found to develop more severe EAE than mice expressing this protein. This was associated with an increased number of immune cells known as Th17 cells in their central nervous system.
Further experiments showed that disease could be alleviated in these mice by administration of a soluble molecule known as IL-27. The authors thus suggest that in individuals with MS, the beneficial effects of IFN-beta are likely to be mediated, at least in part, through its ability to induce the secretion of IL-27.
The study was published in the April 1 issue of the Journal of Clinical Investigation.