Division of Rheumatology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy.
Mol Med. 2010 Nov-Dec;16(11-12):552-7. doi: 10.2119/molmed.2010.00067. Epub 2010 Aug 2.
Tumor necrosis factor-α (TNF-α) is the major target of the therapeutic approach in rheumatoid arthritis. A key issue in the approach to chronic arthritis is the understanding of the crucial molecules driving the transition from the acute phase to the chronic irreversible phase of the disease. In this review we analyzed five experimental arthritis animal models (antigen-induced arthritis, adjuvant-induced arthritis, streptococcal cell wall arthritis, collagen-induced arthritis and SKG) considered as possible scenarios to facilitate interpretation of the biology of human rheumatoid arthritis. The SKG model is strictly dependent on interleukin (IL)-6. In the other models, IL-1β and IL-6, more than TNF-α, appear to be relevant in driving the transition, which suggests that these should be the targets of an early intervention to stop the course toward the chronic form of the disease.
肿瘤坏死因子-α(TNF-α)是类风湿关节炎治疗方法的主要靶点。在慢性关节炎的治疗方法中,一个关键问题是理解驱动疾病从急性期向慢性不可逆期转变的关键分子。在这篇综述中,我们分析了五个实验性关节炎动物模型(抗原诱导关节炎、佐剂诱导关节炎、链球菌细胞壁关节炎、胶原诱导关节炎和 SKG),认为这些模型可能有助于解释人类类风湿关节炎的生物学。SKG 模型严格依赖于白细胞介素(IL)-6。在其他模型中,IL-1β 和 IL-6 比 TNF-α 更能促进疾病的发展,这表明这些应该是早期干预的目标,以阻止疾病向慢性形式发展。