Researchers from the Yale School of Medicine and colleagues at the Massachusetts Institute of Technology (MIT) reported that auto-reactive T-cells in patients with multiple sclerosis (MS) produce different types of cytokines than they do in healthy patients. The study was funded by the National Institutes of Health and the National Multiple Sclerosis Society.
Prior evidence had supported the theory that MS is an autoimmune disease, but the same T-cells that attack the myelin sheath around the nerve cells were found in healthy patients as well. Yale researchers explored this further by analyzing T-cell populations from patients with MS (n=23) and healthy controls (n=22). They found that transcriptomes of myelin-specific CCR6+ T-cells from patients with MS were different from those derived from healthy controls and were enriched in T-helper cell 17 (TH17)-induced experimental autoimmune encephalitis gene signatures.
Researchers concluded that the same mechanism might be present in other autoimmune diseases (eg, rheumatoid arthritis, type 1 diabetes). The functional differences seen in antigen-specific T-cells from MS vs. healthy controls are important to disease development and further supports that interleukin (IL)-10 production from myelin-reactive T-cells may limit disease progression or pathogenesis.
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