Interferon-β exacerbates Th17-mediated inflammatory disease

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 pa...

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Bibliographic Details
Published in:Trends in immunology 2011-06, Vol.32 (6), p.272-277
Main Authors: Axtell, Robert C, Raman, Chander, Steinman, Lawrence
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Autoimmune Diseases - immunology
biomarkers
colitis
Humans
immune response
Inflammation - drug therapy
Inflammation - immunology
interferon-beta
Interferon-beta - immunology
Interferon-beta - therapeutic use
lupus erythematosus
Models, Immunological
patients
psoriasis
rheumatoid arthritis
sclerosis
Th17 Cells - drug effects
Th17 Cells - immunology
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Summary: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.
ISSN:1471-4906
1471-4981
DOI:10.1016/j.it.2011.03.008