title: 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.
authors.affiliation: Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305, USA. axterobe@stanford.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Axtell
authors.forename: Chander
authors.initials: C
authors.lastname: Raman
authors.forename: Lawrence
authors.initials: L
authors.lastname: Steinman
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology; D016899:Interferon-beta / Q000276:immunology* / Q000627:therapeutic use; D018448:Models, Immunological; D058504:Th17 Cells / Q000187:drug effects / Q000276:immunology*
chemical_list: D016899:Interferon-beta