News GM-CSF Cytokine Production Contributes to Multiple Sclerosis Development GM-CSF Cytokine Production Contributes to Multiple Sclerosis Development by Patricia Inacio, PhD | May 1, 2015 Share this article: Share article via email Copy article link In a recent study entitled āExpression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-Ī² Therapy,ā researchers unraveled a key role for theĀ cytokine GM-CSFĀ in multiple sclerosis progression, suggesting GM-CSF asĀ a target of IFN-Ī² therapy. The study was published in The Journal of Immunology. Multiple sclerosis (MS) is a chronic autoimmune disease characterized by aĀ patient’s own immune system attacking theĀ central nervous system, specifically myelin, a component that insulates nerve fibers and maintains a current of neuronal signals. Immune cells release chemical signals called cytokines that act as messengers and chemoattractants for other immune cells, driving inflammation in the brain and contributing to disease progression, marked by neuron death. However, while cytokines are a known established factor in the pathogenesis of MS, which cytokines are the driver of MS has remained a matter of debate. In this study, a team of researchers followed their previous results suggesting that a specific subset of T cells,Ā Th-17 cells, produced a cytokine ā GM-CSF (short for Granulocyte Macrophage Colony-Stimulating Factor) ā that was key inĀ triggering brain inflammation. Moreover, in mouse models of MS disease, the team discovered that those unable to produce GM-CSF never developed the disease. As such, researchersĀ determined if the same effect was observed in human patients with MS and howĀ IFN-therapy, a commonly used treatment, impacted GM-CSF production. The team assessed GM-CSF expression in blood samples of MS patients treated with IFN-Ī² and in those left untreated. Additionally, they also determined GM-CSF production in brain lesions of deceased MS patients and compared those with MS-untreated patients and healthy individuals. They found that untreated patients had significantly higher numbers of GM-CSF producing T cells when compared to IFN-Ī²ātreated MS patients or healthy individuals. The same was observed in brain samples, with increased numbers of GM-CSF-producing cells in MS patients. [adrotate group=”4″] According to the authors, theseĀ findings show increased GM-CSF production contributes to MS pathogenesis and suggests that IFN-Ī² therapy may benefit MS patients by inhibiting GM-CSF expression. Importantly,Ā the preliminary result of a recent Phase 1 clinical trial showed thatĀ antibody-blocking GM-CSF may benefit MS patients. Study lead authorĀ Abdolmohamad Rostami, M.D., Ph.D., Chair of the Department of Neurology at Thomas Jefferson UniversityĀ commented, “After our animal studies showed that GM-CSF was important in the development of an MS-like disease, we were excited to see these results confirmed using samples from MS patients in the current study. We hope that this research showing GM-CSF is an important target will lead us toward therapies that more effectively block the damaging immune reaction in the central nervous system of MS patients.” Print This Page About the Author Patricia Inacio, PhD Patricia holds her PhD in cell biology from the University Nova de Lisboa, Portugal, and has served as an author on several research projects and fellowships, as well as major grant applications for European agencies. She also served as a PhD student research assistant in the Department of Microbiology & Immunology, Columbia University, New York, for which she was awarded a Luso-American Development Foundation (FLAD) fellowship. Tags GM-CSF, multiple sclerosis
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