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Type II collagen-induced arthritis in rats. Passive transfer with serum and evidence that IgG anticollagen antibodies can cause arthritis

机译:II型胶原诱导的大鼠关节炎。血清的被动转移以及IgG抗胶原蛋白抗体可引起关节炎的证据

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摘要

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.
机译:我们发现,用50%硫酸铵分级分离并浓缩后,来自II型胶原诱导的关节炎大鼠的血清会将关节炎转移至未免疫的接受者。接受者的关节炎在18-72 h内发展,并显示了免疫动物早期病变的所有主要组织病理学特征,但是暂时性的,程度较轻。尽管考虑了涉及循环免疫复合物的可能性,但是没有检测到这种复合物的证据。血清的进一步分级产生在转移疾病中完全有活性的IgG抗胶原蛋白抗体。抗体的反应受到用于免疫供体的天然牛II型胶原蛋白的抑制,并且该抗体与同源II型胶原蛋白强烈交叉反应,但与变性胶原蛋白没有交叉反应。这些研究表明,抗II型胶原蛋白抗体可诱发大鼠关节炎,并提示涉及自身免疫过程。由于在人类风湿病中也已经检测到针对胶原蛋白的抗体,因此似乎有必要进一步研究能够诱导关节炎的胶原蛋白抗体的特性。

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  • 年度 1982
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