Trentham D E, McCune W J, Susman P, David J R
J Clin Invest. 1980 Nov;66(5):1109-17. doi: 10.1172/JCI109940.
Arthritis can be induced in rats by intradermal injection of oil containing bacterial derivatives (adjuvant-induced arthritis) or cartilage collagen (type II collagen-induced arthritis). It was of interest, therefore, to determine whether collagen functions as an autoantigen in rats with adjuvant arthritis. Blood mononuclear cells from the majority of rats with adjuvant arthritis exhibited enhanced thymidine incorporation to homologous types I and II collagens, as well as to purified protein derivative of tuberculin. In contrast, cells from rats remaining nonarthritic after injection of adjuvant did not respond to collagen, although they did react to tuberculin. Similar results were obtained with a radiometric ear assay used to quantify intradermal delayed-type hypersensitivity in vivo. Using passive hemagglutination, autoantibodies to these collagens and their denatured alpha-chains were frequently detected in the sera of rats late in the course of adjuvant arthritis. Rats with inflammation of a hindlimb induced by turpentine did not acquire sensitivity to collagen. These data indicate that autoimmunity to collagen is a common feature of adjuvant- and collagen-induced arthritis, both of which are considered to be mediated by immunologic mechanisms.
通过皮内注射含有细菌衍生物的油（佐剂诱导的关节炎）或软骨胶原蛋白（II型胶原诱导的关节炎）可在大鼠中诱发关节炎。因此，确定胶原蛋白在佐剂性关节炎大鼠中是否作为自身抗原发挥作用很有意义。大多数佐剂性关节炎大鼠的血液单核细胞对同源的I型和II型胶原蛋白以及结核菌素纯蛋白衍生物表现出增强的胸腺嘧啶核苷掺入。相比之下，注射佐剂后仍未患关节炎的大鼠的细胞对胶原蛋白无反应，尽管它们对结核菌素起反应。使用用于在体内定量皮内迟发型超敏反应的放射性耳测定法也获得了类似结果。通过被动血凝试验，在佐剂性关节炎病程后期的大鼠血清中经常检测到针对这些胶原蛋白及其变性α链的自身抗体。由松节油诱导后肢炎症的大鼠对胶原蛋白不产生敏感性。这些数据表明，对胶原蛋白的自身免疫是佐剂诱导和胶原诱导的关节炎的共同特征，这两种关节炎都被认为是由免疫机制介导的。
