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Published on: August 10, 2018
Recombinant interferon-beta therapy and neuromuscular disorders
1Department of Neurology and Neuroscience, Weill Medical College of Cornell University/New York Presbyterian Hospital, New York, NY 10065-4885, USA. pstuebge@med.cornell.edu
Interferon-beta (IFNbeta) is an extra-cellular protein mediator of host defense and homeostasis. IFNbeta has well-established direct antiviral, antiproliferative and immunomodulatory properties. Recombinant IFNbeta is approved for the treatment of relapsing-remitting multiple sclerosis. The immunomodulatory effects of IFNbeta 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 IFNbeta therapy, and the relatively brief periods of IFNbeta 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. IFNbeta therapy may trigger autoantibody production, but only rarely clinically overt autoimmune disease. Anecdotal reports hint at the exceptional association between IFNbeta treatment and the induction or exacerbation of a variety of immune-mediated neuromuscular diseases, likely in genetically predisposed individuals. Thus, recombinant IFNbeta has the theoretical potential to either treat or cause autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks.
Interferon-beta (IFNbeta) is an extra-cellular protein mediator of host defense and homeostasis. IFNbeta has well-established direct antiviral, antiproliferative and immunomodulatory properties. Recombinant IFNbeta is approved for the treatment of relapsing-remitting multiple sclerosis. The immunomodulatory effects of IFNbeta 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 IFNbeta therapy, and the relatively brief periods of IFNbeta 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. IFNbeta therapy may trigger autoantibody production, but only rarely clinically overt autoimmune disease. Anecdotal reports hint at the exceptional association between IFNbeta treatment and the induction or exacerbation of a variety of immune-mediated neuromuscular diseases, likely in genetically predisposed individuals. Thus, recombinant IFNbeta has the theoretical potential to either treat or cause autoimmune neuromuscular disorders by altering the complicated and delicate balances within the immune system networks.
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