Reporting online on April 24, 2011, in Nature Immunology, Jefferson Medical College neuroscientists have identified a driving force behind autoimmune diseases such as multiple sclerosis (MS), and suggest that blocking this cell-signaling molecule is the first step in developing new treatments to eradicate these diseases. Researchers led by Dr. Abdolmohamad Rostami, Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, found that GM-CSF, which stands for granulocyte-macrophage colony-stimulating factor, appears to be the key culprit in the onset of MS, because without it, T helper 17 (Th17) cells did not induce the MS-like disease in an experimental animal model. Th17 cells have been shown to play an important pathogenic role in humans and experimental models of autoimmune diseases, but the mechanisms behind this have remained elusive until now. "There was no connection between GM-CSF and Th17 cells before," said Dr. Rostami. "What we have shown in this paper is that GM-CSF derived from Th17 cells is important in the cell-signaling process that leads to inflammation in the central nervous system. Now we know how the Th17 cells work and a better understanding of this mechanism and biology leads to new therapeutics," he added. The results suggest that blocking GM-CSF activity may be a successful therapeutic strategy in MS, one of the most common neurological diseases affecting young adults, and other autoimmune diseases, said Dr. Rostami, who is also the Chair of Neurology at Thomas Jefferson University Hospital. These findings identify the interleukin-23 (IL-23)/ Th17/GM-CSF axis as the major pathway in pathogenesis of autoimmune central nervous system inflammation and likely other autoimmune diseases.
Login Or Register To Read Full Story