Mozes E, Brocke S, Shoenfeld Y, Mendlovic S
Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.
J Cell Biochem. 1989 Jun;40(2):173-81. doi: 10.1002/jcb.240400206.
Systemic lupus erythematosus (SLE) has been induced in C3H.SW mice by their immunization with a human monoclonal anti-DNA antibody that bears a common idiotype-16/6 Id. Following immunization, high levels of murine anti-16/6 and anti-anti-16/6 antibodies were detected in the sera of the immunized mice. Elevated titers of autoantibodies reacting with ssDNA, dsDNA, poly(I), poly(G), RNP, Ro, and La were also observed. The serological findings were associated with significant proteinuria, leukopenia, and elevated erythrocyte sedimentation rate. Immune complex deposition in the glomerular mesangium and sclerosis of the glomeruli were demonstrated. To study whether or not anti-idiotype antibodies are involved in the induction of the disease, a murine monoclonal antibody against the 16/6 Id was prepared and injected into C3H.SW mice. The anti-16/6 Id antibody induced experimental SLE similarly to the 16/6 Id with an accelerated kidney pathology. A study performed on different mouse strains indicated that the susceptibility to the induction of SLE by the 16/6 Id is strain dependent and directly correlates to their ability to produce anti-16/6 Id specific antibodies.
用携带共同独特型16/6 Id的人单克隆抗DNA抗体免疫C3H.SW小鼠可诱导出系统性红斑狼疮(SLE)。免疫后,在免疫小鼠的血清中检测到高水平的鼠抗16/6和抗抗16/6抗体。还观察到与单链DNA、双链DNA、聚肌苷酸、聚鸟苷酸、核糖核蛋白、Ro和La反应的自身抗体滴度升高。血清学结果与明显的蛋白尿、白细胞减少和红细胞沉降率升高有关。证实了免疫复合物在肾小球系膜中的沉积和肾小球硬化。为了研究抗独特型抗体是否参与疾病的诱导,制备了一种针对16/6 Id的鼠单克隆抗体并将其注射到C3H.SW小鼠体内。抗16/6 Id抗体诱导的实验性SLE与16/6 Id相似,但肾脏病理改变加速。对不同小鼠品系进行的一项研究表明,16/6 Id诱导SLE的易感性具有品系依赖性,并且与其产生抗-16/6 Id特异性抗体的能力直接相关。