Nordling C, Kleinau S, Klareskog L
Department of Clinical Immunology, University Hospital, Uppsala, Sweden.
Immunology. 1992 Sep;77(1):144-6.
We recently described a spontaneously occurring, inflammatory and erosive joint disease in male DBA/1 mice. A major question is whether specific immune reactions are involved in eliciting this disease. The possibility that collagen autoimmunity might constitute one pathogenic factor was particularly interesting as this spontaneous arthritis appears to be genetically restricted in a way similar to collagen-induced arthritis. In the present study, we demonstrate increased serum antibody levels to collagen II in a fraction of the male DBA/1 mice, but not in age-matched female controls. Administration of antibodies with an anti-idiotypic activity to anti-collagen II antibodies and with an affinity for determinants present on isolated syngeneic IgG Fc but not on intact IgG, was shown to interfere with the development of the spontaneous arthritis in a manner similar to that earlier documented for collagen arthritis. These observations suggest that mechanisms similar to those operating in collagen-induced arthritis may also be found in the spontaneously occurring arthritis in male DBA/1 mice.
我们最近描述了一种在雄性DBA/1小鼠中自发出现的炎性侵蚀性关节疾病。一个主要问题是特定的免疫反应是否参与引发这种疾病。胶原自身免疫可能构成一个致病因素,这一可能性特别有趣,因为这种自发性关节炎似乎在遗传上受到限制,其方式类似于胶原诱导的关节炎。在本研究中,我们证明了一部分雄性DBA/1小鼠血清中抗II型胶原抗体水平升高,但年龄匹配的雌性对照小鼠中未出现这种情况。向抗II型胶原抗体注射具有抗独特型活性且对分离的同基因IgG Fc上存在但完整IgG上不存在的决定簇具有亲和力的抗体,结果显示其能以类似于先前记录的胶原性关节炎的方式干扰自发性关节炎的发展。这些观察结果表明,在雄性DBA/1小鼠的自发性关节炎中,可能也存在与胶原诱导性关节炎中起作用的机制类似的机制。