TYPE-II COLLAGEN-INDUCED ARTHRITIS IN RATS - PASSIVE TRANSFER WITH SERUM AND EVIDENCE THAT IGG ANTI-COLLAGEN ANTIBODIES CAN CAUSE ARTHRITIS

TYPE-II COLLAGEN-INDUCED ARTHRITIS IN RATS - PASSIVE TRANSFER WITH SERUM AND EVIDENCE THAT IGG ANTI-COLLAGEN ANTIBODIES CAN CAUSE ARTHRITIS
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DOI:
10.1084/jem.155.1.1
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发表时间:
1982-01-01
影响因子:
15.3
通讯作者:
KANG, AH
KANG, AH
中科院分区:
医学1区
文献类型:
--
作者:
STUART, JM;CREMER, MA;KANG, AH

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从II型胶原诱导的关节炎大鼠的血清,当用50%硫酸铵分级和浓缩,转移关节炎到非免疫受体。受者的关节炎在18-72小时内发生,并显示免疫动物早期病变的所有主要组织病理学特征,但短暂且不太严重。尽管考虑了涉及循环免疫复合物的可能性,但没有检测到这种复合物的证据。血清的进一步分级分离产生在转移疾病中完全活跃的IgG抗胶原抗体。抗体的反应被用于免疫供体的天然牛II型胶原抑制,并且抗体与同源II型胶原强烈交叉反应,但不与变性胶原交叉反应。抗II型胶原抗体可以诱导大鼠关节炎,这表明涉及自身免疫过程。由于在人类风湿性疾病中也检测到胶原抗体,因此有必要进一步研究能够诱导关节炎的胶原抗体的特征。
Serum from rats with type II collagen-induced arthritis, when fractionated with 50% ammonium sulfate and concentrated, transfered 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 collagen but not with denatured collagen. That arthritis in rats can be induced with anti-type II collagen antibodies suggests 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.