Although the drug IFN-beta is commonly used to treat individuals with the relapsing-remitting form of multiple sclerosis (MS), little is known about the mechanism(s) by which it acts. However, Genhong Cheng and colleagues, at the University of California at Los Angeles, have now reported a mechanistic pathway by which it reduces disease in a mouse model of MS known as EAE.
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 to mediate its effects were found to develop more severe EAE than mice expressing this protein. This was associated with increased numbers of immune cells known as Th17 cells in the central nervous system of the mice, the part of the body affected in individuals with MS. Further experiments showed that disease could be alleviated in these mice by administration of a soluble molecule known as IL-27, leading the authors to 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.
TITLE: The type I IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice
AUTHOR CONTACT:
Genhong Cheng
University of California at Los Angeles, Los Angeles, California, USA.
Phone: (310) 825-8896; Fax: (310) 206-5553. Email: genhongc@microbio.ucla.edu.
View the PDF of this article at: https://www.the-jci.org/article.php?id=33342
Journal
Journal of Clinical Investigation