Fenner H
Z Rheumatol. 1995 May-Jun;54(3):158-64.
Interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF alpha) have been identified as important mediators of chronic immuno-inflammatory disease states such as rheumatoid arthritis. Effector cells are triggered by these cytokines to release molecules involved in synovitis and rheumatoid joint destruction, namely prostanoids, leukotrienes, adhesion molecules and metalloproteinases. Modifications of natural inhibitors of IL-1 and TNF alpha, which have been shown to maintain the homeostasis of the cytokine system, are now available by DNA technology. Monoclonal antibodies to TNF and the TNF receptor fusion proteins TNFR 55-IgG and TNFR 75-IgG are currently under clinical investigation in rheumatoid arthritis, inflammatory bowel disease and septic shock. Preliminary results from clinical trials in rheumatoid arthritis suggest that TNF inhibition represents a promising novel interventional strategy providing anti-inflammatory activity and inhibition of effector molecules of structural joint damage.
白细胞介素1(IL-1)和肿瘤坏死因子α(TNFα)已被确定为类风湿关节炎等慢性免疫炎症性疾病状态的重要介质。效应细胞被这些细胞因子触发,释放参与滑膜炎和类风湿关节破坏的分子,即前列腺素、白三烯、黏附分子和金属蛋白酶。现已通过DNA技术对IL-1和TNFα的天然抑制剂进行修饰,这些抑制剂已被证明可维持细胞因子系统的稳态。针对TNF的单克隆抗体以及TNF受体融合蛋白TNFR 55-IgG和TNFR 75-IgG目前正在类风湿关节炎、炎症性肠病和感染性休克的临床试验中进行研究。类风湿关节炎临床试验的初步结果表明,抑制TNF代表了一种有前景的新型干预策略,可提供抗炎活性并抑制结构性关节损伤的效应分子。