Encephalomyelitis
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New findings in multiple sclerosis described by L. Durelli and co-researchers
2009 JUL 20 - (NewsRx.com) -- According to recent research from Turin, Italy, "T-helper 1 (Th1) and Th17 lymphocytes are involved in experimental autoimmune encephalomyelitis, the model of multiple sclerosis (MS). We characterized the Th1/Th17 cell population in peripheral blood (PB), their interferon (IFN) receptor expression sensitivity to IFN-beta in MS patients." "In 30 untreated patients with active MS (AMS) and 32 with inactive MS (IMS), and in 22 healthy subjects, we measured intracellular cytokine expression, interleukin-17-producing myelin basic protein-stimulated PB lymphocytes, surface IFN type I receptor chain 1 (IFN-alpha R1) expression, IFN-beta-dependent signal transducer and activator of transcription 1 (STAT1) phosphorylation, and apoptosis of anti-CD3 monoclonal antibody-stimulated PB lymphocytes. Th17 cell percentage increased around sevenfold in AMS compared with IMS or healthy Subjects, but there was no change in Th1 cells. Th17 cells in AMS were myelin basic protein specific. The longitudinal follow-up of 18 MS patients shifting between AMS and IMS showed that the percentage of Th17 but not Th1 cells always increased in AMS. IFN-alpha R1 expression, IFN-beta-induced STAT1 activation, and apoptosis were significantly greater in Th17 than Th1 cells. IFN-alpha R1 expression and IFN-beta-dependent STAT1 activation progressively increased in vitro with a highly significant positive correlation only in developing Th17 but not in Th0 or Th1 cells. Evidence that an expansion of peripheral Th17 cells, a Th Subset chat can infiltrate brain parenchyma and damage cells, is associated with disease activity in MS," wrote L. Durelli and colleagues. The researchers concluded: "The greater IFN-alpha R1 level expressed by Th17 compared with Th1 cells might make them a selective target for IFN-beta therapy." Durelli and colleagues published their study in Annals of Neurology (T-Helper 17 Cells Expand in Multiple Sclerosis and Are Inhibited by Interferon-beta. Annals of Neurology, 2009;65(5):499-509). For additional information, contact F. Novelli, San Giovanni Battista Hospital, Center Experimental Research & Med Studies, Via Cherasco N 15, I-10127 Turin, Italy. Publisher contact information for the journal Annals of Neurology is: Wiley-Liss, Division John Wiley & Sons Inc., 111 River St., Hoboken, NJ 07030, USA. Keywords: Italy, Turin, Apoptosis, Autoimmune Disease, Autoimmune Disorder, Biotechnology, Central Nervous System Disease, Encephalomyelitis, Experimental Autoimmune Encephalomyelitis, Immunology, Interferon, Medical Device, Monoclonal Antibody, Multiple Sclerosis, Neuroimmunology, Neurology, Urology. This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2009, Pain & Central Nervous System Week via NewsRx.com.
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