Jefferson University Hospitals Multiple sclerosis (MS) probably treated by a hypertension drug, is triggered by Granulocyte-macrophage colony-stimulating factor (GM-CSF). Jefferson neuroscientists now claim that simply blocking an important molecule can also aid in fighting MS. Obstructing this cell-signaling molecule appears as the first step in developing new treatments to eradicate the disease.

In the absence of GM-CSF, T helper 17 cells (Th17) cells were supposedly unable to induce the MS-like disease in an experimental animal model. Th17 cells are believed to play a vital pathogenic role in humans and experimental models of autoimmune diseases, but the mechanisms behind this are hazy. In the course of the research, it was suggested that GM-CSF derived from Th17 cells is important in the cell-signaling process that leads to inflammation in the central nervous system.

The interleukin-23 (IL-23)/ Th17/GM-CSF axis seem to be the major pathway in pathogenesis of autoimmune central nervous system inflammation and likely other autoimmune diseases. IL-23 may be a cytokine that leads to autoimmune inflammation of the brain, induces production of more GM-CSF in Th17 cells. An animal model of MS called experimental autoimmune encephalomyelitis (EAE) was used for the investigation.

Abdolmohamad Rostami, M.D., Ph.D., Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, added, “This is the first step towards finding a new treatment. If we can try to neutralize GM-CSF by different means, for example, by trying to mimic it or trying to block the receptor for GM-CSF, we can hopefully ameliorate the disease.”

Mice whose Th17 cells cannot produce GM-CSF possibly failed to develop neuroinflammation. Hence, it can be asserted that GM-CSF is responsible for disease manifestation in this experimental model. Scientists found that the protein interkeukin-27 (IL-27) helped block the onset of symptoms in animals with an MS-like disease. Increasing levels of GM-CSF can trigger the disease, while elevating IL-27 concentrations can supposedly suppress an over-active immune system.

The research is published in Nature Immunology.