A new study recently published in the journal Science Translational Medicine revealed a key difference in immune T cells between multiple sclerosis (MS) patients and healthy individuals. The study is entitled “Functional inflammatory profiles distinguish myelin-reactive T cells from patients with multiple sclerosis” and was led by researchers at Yale School of Medicine, Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology (MIT) and The Broad Institute of MIT and Harvard.
MS is a progressive neurodegenerative autoimmune disorder that results from an attack on the central nervous system by the body’s own immune system, causing inflammation and damage to the myelin layer that covers and protects nerve fibers. Myelin loss leads to impairment in signal transmission along the nerve fibers, affecting motor function (like coordination, balance, speech and vision), causing irreversible neurological disability and paralysis. It is estimated that more than 2.3 million people in the world suffer from the disease.
Immune T cells were found to be involved in the attack to the myelin layer around nerve cells in MS patients. These same T cells are also present in healthy individuals with comparable frequencies, suggesting that there must be something different in the context of the disease.
In this study, researchers examined the T cell population of 23 MS patients and 22 healthy controls for reactivity against myelin. The team found that myelin-reactive T cells from MS patients had an increased production of proinflammatory cytokines (molecules important in cell signaling that promote inflammation), including interferon-gamma, interleukin-17 and granulocyte-macrophage colony-stimulating factor (GM-CSF), in comparison to healthy controls. Based on these findings, the team suggested that these differences in the inflammatory profile of T cells between MS patients and healthy individuals are a key factor for disease development.
The research team concluded that the auto-reactive T cells in MS patients generate different types of inflammatory cytokines in comparison to the cytokines that they produce in healthy individuals. “In most people, these T cells are acting to repair tissue, but in MS patients, they do damage to the nervous system,” explained the study’s senior author Dr. David Hafler in a news release.
The team proposes that drugs against these inflammatory cytokines could potentially be considered a promising therapy for MS. The team also suggests that a similar effect may occur in other autoimmune diseases, like type 1 diabetes and rheumatoid arthritis.
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