Stuart J M, Cremer M A, Townes A S, Kang A H
J Exp Med. 1982 Jan 1;155(1):1-16. doi: 10.1084/jem.155.1.1.
We have found that serum from rats with type II collagen-induced arthritis, when fractionated with 50% ammonium sulfate and concentrated, would transfer arthritis to nonimmunized recipients. The arthritis in recipients developed within 18-72 h and displayed all of the major histopathologic characteristics of the early lesion in immunized animals but was transient and less severe. Although consideration was given to the possibility that a circulating immune complex was involved, no evidence of such a complex was detected. Further fractionation of the serum yielded an IgG anticollagen antibody that was fully active in transferring disease. The antibody's reaction was inhibited by the native bovine type II collagen used for immunization of donors and the antibody strongly cross-reacted with homologous type II collage but not with denatured collagen. These studies demonstrate that arthritis in rats can be induced with anti-type II collagen antibodies and suggest that an autoimmune process is involved. Because antibodies to collagen have also been detected in human rheumatic diseases, further investigation of the characteristics of collagen antibodies capable of inducing arthritis seems warranted.
我们发现，用50%硫酸铵分级分离并浓缩的II型胶原诱导性关节炎大鼠血清，可将关节炎转移至未免疫的受体。受体中的关节炎在18 - 72小时内出现，表现出免疫动物早期病变的所有主要组织病理学特征，但具有短暂性且症状较轻。尽管考虑了循环免疫复合物参与的可能性，但未检测到此类复合物的证据。血清的进一步分级分离产生了一种IgG抗胶原抗体，该抗体在转移疾病方面具有完全活性。该抗体的反应被用于免疫供体的天然牛II型胶原所抑制，并且该抗体与同源II型胶原强烈交叉反应，但与变性胶原不发生反应。这些研究表明，大鼠的关节炎可由抗II型胶原抗体诱导，并提示涉及自身免疫过程。由于在人类风湿性疾病中也检测到了抗胶原抗体，因此似乎有必要进一步研究能够诱导关节炎的胶原抗体的特征。
