首页> 美国卫生研究院文献>Molecular Medicine >Interleukin-1β and Interleukin-6 in Arthritis Animal Models: Roles in the Early Phase of Transition from Acute to Chronic Inflammation and Relevance for Human Rheumatoid Arthritis
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Interleukin-1β and Interleukin-6 in Arthritis Animal Models: Roles in the Early Phase of Transition from Acute to Chronic Inflammation and Relevance for Human Rheumatoid Arthritis

机译:白细胞介素1β和白细胞介素6在关节炎动物模型中的作用:从急性炎症过渡到慢性炎症的早期阶段和与人类类风湿关节炎的相关性。

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摘要

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.
机译:肿瘤坏死因子-α(TNF-α)是类风湿关节炎治疗方法的主要目标。慢性关节炎治疗方法中的一个关键问题是对驱动该疾病从急性期过渡到慢性不可逆期的关键分子的了解。在这篇综述中,我们分析了五种实验性关节炎动物模型(抗原诱导的关节炎,佐剂诱导的关节炎,链球菌细胞壁关节炎,胶原蛋白诱导的关节炎和SKG),它们被认为是有助于人类类风湿性关节炎生物学解释的可能方案。 SKG模型严格依赖于白介素(IL)-6。在其他模型中,IL-1β和IL-6(而不是TNF-α)似乎与推动这一转变有关,这表明这些应该成为早期干预的目标,以阻止其朝慢性形式发展。疾病。

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