Interferon-β exacerbates Th17-mediated inflammatory disease

被引：90

作者：

Axtell, Robert C. ^{[1
]}

Raman, Chander ^{[2
]}

Steinman, Lawrence ^{[1
]}

机构：

[1] Stanford Univ, Dept Neurol & Neurol Sci, Interdept Program Immunol, Stanford, CA 94305 USA

[2] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 06期

关键词：

REMITTING MULTIPLE-SCLEROSIS; NEW-ONSET PSORIASIS; T-HELPER TYPE-1; NEUROMYELITIS-OPTICA; IFN-GAMMA; RHEUMATOID-ARTHRITIS; TH17; CELLS; DISTINCT; CYTOKINE; ANTIBODY;

D O I：

10.1016/j.it.2011.03.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：272 / 277

页数：6

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