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Interferon-β exacerbates Th17-mediated inflammatory disease

Journal

TRENDS IN IMMUNOLOGY
Volume 32, Issue 6, Pages 272-277

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.it.2011.03.008

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Funding

  1. NIAID NIH HHS [R21 AI095055, R01 AI076562] Funding Source: Medline
  2. NINDS NIH HHS [R01 NS055997] Funding Source: Medline

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Interferon (IFN)-beta is the treatment most often prescribed for relapsing-remitting multiple sclerosis (RRMS). 30-50% of MS patients, however, do not respond to IFN-beta. In some cases, IFN-beta exacerbates MS, and it consistently worsens neuromyelitis optica (NMO). To eliminate unnecessary treatment for patients who are non-responsive to IFN-beta, 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-beta is ineffective and might worsen clinical status in diverse diseases when a Th17 immune response is prominent.

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