News Potential Mechanism in MS Pathogenesis Seen in Study Potential Mechanism in MS Pathogenesis Seen in Study by Patricia Inacio, PhD | January 6, 2016 Share this article: Share article via email Copy article link Researchers found that a group of untreated patients with multiple sclerosis (MS) and patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) carry a specific group of hyperactivated immune cells, the inflammatory CD8+ T cells, suggesting a potential common mechanism contributing to disease pathogenesis. The study, “A Preliminary Comparative Assessment of the Role of CD8+ T Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis,” was published in the Journal of Immunology Research. The immune system carries a special group of immune cells, called CD8+ T cells, with key functions in regulating immune system responses during an infection. Notably, CD8+ T cells have been identified in central nervous system lesions of MS patients, where they were suggested to contribute to the pro-inflammatory environment. MS is an immune-mediated disease of the central nervous system characterized by destruction of the myelin layer within nerve cells, leading to a wide range of neurological symptoms. Recent studies reported that some MS patients develop CFS/ME, evidenced by a significant impairment in patients’ physical activity as a consequence of severe fatigue. Since immune dysregulation is a common feature of both CFS/ME and MS, researchers investigated the levels and maturation of CD8+ T cells in serum samples collected from 23 CFS/ME patients, 11 MS patients without any history of immunomodulatory therapy, and 30 non-fatigued controls. To identify the subsets of CD8+ T cells at different stages of differentiation, researchers used stage-specific monoclonal antibodies. The team found that CFS/ME and MS patients exhibited a significant impairment in several subsets of CD8+ T cells, with MS patients showing a particularly significant differential expression of several surface receptors within subsets. The findings suggest that untreated MS patients may carry hyperactivated inflammatory CD8+ T cells as a result of major deficits in the expression of receptors and adhesion molecules on subsets of this cell population. The same phenotype was observed in CFS/ME patients (although MS patients seem to carry more severe immune dysregulation), suggesting that these deficits are a potential underlying mechanism contributing to the pathogenesis of these diseases. Further studies with larger cohorts of patients are, however, necessary to confirm these preliminary findings. 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 myelin
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