Pathogenesis of rheumatoid arthritis: Targeting cytokines

被引:122
作者
Zwerina, J [1 ]
Redlich, K [1 ]
Schett, G [1 ]
Smolen, JS [1 ]
机构
[1] Med Univ Vienna, Div Rheumatol, A-1090 Vienna, Austria
来源
AUTOIMMUNE DISEASES AND TREATMENT: ORGAN-SPECIFIC AND SYSTEMIC DISORDERS | 2005年 / 1051卷
关键词
rheumatoid arthritis; cytokines; TNF; IL-1; IL-6; IL-15; disease activity; joint damage; osteoclasts; therapy; anti-TNF; IL-1ra; anti-IL-6R (MRA);
D O I
10.1196/annals.1361.116
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Although considerable progress has been made by adequate treatment with traditional disease-modifying antirheumatic drugs (DMARDs), therapy of rheumatoid arthritis (RA) still remains difficult. The discovery of the importance of cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-15 (IL-15), which are also stimulated by consequences of autoimmune responses, has led to the development of anticytokine therapies ("biologicals"). Blocking TNF or also, to some extent, IL-1 has proved beneficial in DMARD-resistant RA patients in multiple clinical trials. Along with clinical improvement, TNF blockade has been shown to halt radiographic disease progression, a major risk factor for disability. Recently, clinical trials have shown a significant therapeutic benefit of biological inhibitors of IL-6, and also of IL-15, with an efficacy comparable to that of TNF blockers. All these agents are particularly efficacious when combined with methotrexate. Although clinical remission is difficult to achieve even with anticytokine treatment, these drugs offer the potential to decrease disease activity and improve quality of life in a majority of RA patients, and it is conceivable that combinations of biological therapies may pave the path to even better success, which ultimately is remission or even cure.
引用
收藏
页码:716 / 729
页数:14
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