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Interferon-β exacerbates Th17-mediated inflammatory disease.

Abstract
Interferon (IFN)-β is the treatment most often prescribed for relapsing-remitting multiple sclerosis (RRMS). 30-50% of MS patients, however, do not respond to IFN-β. In some cases, IFN-β exacerbates MS, and it consistently worsens neuromyelitis optica (NMO). To eliminate unnecessary treatment for patients who are non-responsive to IFN-β, and to avoid possible harm, researchers are identifying biomarkers that predict treatment outcome before treatment is initiated. These biomarkers reveal insights into the mechanisms of disease. Recent discoveries on human samples from patients with RRMS, NMO, psoriasis, rheumatoid arthritis, systemic lupus erythematosus and ulcerative colitis, indicate that IFN-β is ineffective and might worsen clinical status in diverse diseases when a Th17 immune response is prominent.
AuthorsRobert C Axtell, Chander Raman, Lawrence Steinman
JournalTrends in immunology (Trends Immunol) Vol. 32 Issue 6 Pg. 272-7 (Jun 2011) ISSN: 1471-4981 [Electronic] England
PMID21530402 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2011 Elsevier Ltd. All rights reserved.
Chemical References
  • Interferon-beta
Topics
  • Animals
  • Autoimmune Diseases (immunology)
  • Humans
  • Inflammation (drug therapy, immunology)
  • Interferon-beta (immunology, therapeutic use)
  • Models, Immunological
  • Th17 Cells (drug effects, immunology)

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