Kerwar S S, Oronsky A L
Int J Tissue React. 1985;7(6):409-29.
Immunization of laboratory rats with native Type II collagen induces arthritis in approximately 40 percent of the individuals. Histological and radiological analysis have suggested that the lesion bears several similarities to human rheumatoid arthritis. Clinical studies conducted with this model indicate that it is responsive to the treatment with clinically-used NSAID'S, steroids and immunosuppressive agents. When rats with collagen arthritis were treated with DMARD's, only those treated with D-penicillamine showed clinical improvement (radiological evaluation). Type II collagen induced arthritis is complement-dependent and is an example of an immune complex mediated injury. Thus, passive arthritis can be induced in rats by the intravenous administration of affinity-purified anticollagen IgG. The passive lesion is transient and the administered IgG is detected on the articular cartilage of the hind paws. This articular cartilage also contains complement C3. Passive arthritis is also complement-dependent. Suppression of Type II collagen arthritis can be induced by the prior intravenous treatment of rats with either Type II collagen or its constituent peptide alpha 1, (II) CB10. Antigen-induced arthritis cannot be induced in those rats that have recovered from passive arthritis.
用天然II型胶原免疫实验大鼠,约40%的个体可诱发关节炎。组织学和放射学分析表明,该病变与人类类风湿关节炎有若干相似之处。用该模型进行的临床研究表明,它对临床使用的非甾体抗炎药、类固醇和免疫抑制剂治疗有反应。当用改善病情抗风湿药治疗胶原性关节炎大鼠时,只有用D -青霉胺治疗的大鼠显示出临床改善(放射学评估)。II型胶原诱导的关节炎是补体依赖性的,是免疫复合物介导损伤的一个例子。因此,通过静脉注射亲和纯化的抗胶原IgG可在大鼠中诱发被动性关节炎。被动性病变是短暂的,在大鼠后爪的关节软骨上可检测到注入的IgG。该关节软骨也含有补体C3。被动性关节炎也是补体依赖性的。用II型胶原或其组成肽α1,(II)CB10预先静脉注射大鼠,可诱导对II型胶原关节炎的抑制。在从被动性关节炎中恢复的大鼠中不能诱发抗原诱导的关节炎。