A new study published in the Journal of Immunology has confirmed that the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF) likely plays a critical role in multiple sclerosis (MS) in humans, and has proposed a new reasoning for why treatment with interferon-beta is often effective in reducing MS attacks.
Th-17 cells became a new focus as it appeared to play a role in neuronal damage progression in MS. This led researchers to believe that cytokine IL-17, produced by Th-17 cells, was also important to MS. However in 2011, researchers from Thomas Jefferson University found that Th-17 cells also produced cytokine GM-CSF, which reacted with another cell type, significantly increasing its levels in the brain of mouse models. In addition, mice that were unable to produce GM-CSF never developed the disease, though mice lacking IL-17 did develop mild disease.
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To assess whether the same observation was true in human disease, researchers tested blood samples of patients with MS who had not received treatment, those who were receiving interferon-beta, or normal subjects. They found that patients who were untreated had 2–3 times as many immune cells producing GM-CSF as did patients being treated with interferon-beta or normal subjects. The team also studied brain samples of deceased patients with MS and discovered increased numbers of GM-CSF-producing cells in comparison to normal brain samples.
Findings support that GM-CSF is an important target and researchers hope future treatments can better block the harmful immune reaction in the central nervous system for these patients.
For more information visit jefferson.edu.