Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065085 | Journal of Neuroimmunology | 2009 | 10 Pages |
Interferon-beta (IFNβ) is an extra-cellular protein mediator of host defense and homeostasis. IFNβ has well-established direct antiviral, antiproliferative and immunomodulatory properties. Recombinant IFNβ is approved for the treatment of relapsing–remitting multiple sclerosis. The immunomodulatory effects of IFNβ administration failed to demonstrate consistent benefit during treatment of various autoimmune neuromuscular diseases. Existing studies were flawed due to the often uncontrolled and unblinded nature of protocols, small patient numbers per study, the undetermined optimum dose and schedule of IFNβ therapy, and the relatively brief periods of IFNβ administration and clinical follow-up for mostly chronic inflammatory disorders. Additional, controlled, prospective studies are needed to definitely establish the full potential of this cytokine for this group of diseases. IFNβ therapy may trigger autoantibody production, but only rarely clinically overt autoimmune disease. Anecdotal reports hint at the exceptional association between IFNβ treatment and the induction or exacerbation of a variety of immune-mediated neuromuscular diseases, likely in genetically predisposed individuals. Thus, recombinant IFNβ has the theoretical potential to either treat or cause autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks.