Linton S M, Morgan B P
Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK.
Mol Immunol. 1999 Sep-Oct;36(13-14):905-14. doi: 10.1016/s0161-5890(99)00113-3.
Complement activation has been implicated as a pathological process in a number of inflammatory and autoimmune disorders including chronic rheumatoid arthritis (RA). Animal models of experimental arthritis have been widely used to investigate the pathogenesis of RA and also in the development of novel therapies. Many of these models are complement-dependent and both incidence and progression of disease can be influenced by complement inhibition. In certain situations, local inhibition is of greater therapeutic benefit than systemic decomplementation. An increasing awareness and availability of a wide range of naturally occurring complement regulatory proteins can now offer a more targeted approach to complement inhibition while the availability of novel engineering strategies has also improved the efficiency of this process. The success of complement inhibition in the experimental models described should offer a novel therapeutic approach to the treatment of human inflammatory arthritis.
补体激活已被认为是包括慢性类风湿性关节炎（RA）在内的多种炎症和自身免疫性疾病中的一种病理过程。实验性关节炎的动物模型已被广泛用于研究RA的发病机制以及新型疗法的开发。这些模型中的许多都是补体依赖性的，疾病的发生率和进展都可能受到补体抑制的影响。在某些情况下，局部抑制比全身补体灭活具有更大的治疗益处。现在，人们对多种天然存在的补体调节蛋白的认识不断提高且其可得性增加，这可以提供一种更具针对性的补体抑制方法，同时新型工程策略的可得性也提高了这一过程的效率。上述实验模型中补体抑制的成功应为人类炎性关节炎的治疗提供一种新的治疗方法。
