Cox K O, Koh L Y
Clin Exp Immunol. 1977 Mar;27(3):560-3.
Mice immunized with cross-reacting rat erythrocytes develop autoimmune haemolytic anaemia as indicated by haematological data and erythrocyte autoantibodies. With continued immunization the mice recover haematologically but remain Coombs' positive. Coombs' tests were performed using monospecific antisera to determine whether the recovery from anaemia was associated with a change in the class or subclass of the autoantibodies produced. In both splenectomized mice and in unsplenectomized mice the following subclass of erythrocyte autoantibodies were present: IgG1, IgG2A, IgG2B. IgA autoantibodies were not detected and IgM autoantibodies were only detected in splenectomized mice 1-3 weeks after the IgG autoantibodies had appeared. After six immunizations the frequency of IgG2B autoantibodies decreased and by the tenth immunization and thereon, IgG2B autoantibodies were not detected. It is proposed from these results that the anaemia is caused by IgG2B autoantibodies and the the sudden exacerbation in the anaemia that occurs in splenectomized mice is due to the production of IgM autoantibodies.
用交叉反应性大鼠红细胞免疫的小鼠出现自身免疫性溶血性贫血,血液学数据和红细胞自身抗体表明了这一点。随着持续免疫,小鼠血液学上恢复,但抗人球蛋白试验仍呈阳性。使用单特异性抗血清进行抗人球蛋白试验,以确定贫血的恢复是否与所产生的自身抗体的类别或亚类变化有关。在脾切除小鼠和未脾切除小鼠中均存在以下红细胞自身抗体亚类:IgG1、IgG2A、IgG2B。未检测到IgA自身抗体,仅在IgG自身抗体出现后1至3周的脾切除小鼠中检测到IgM自身抗体。经过六次免疫后,IgG2B自身抗体的频率降低,到第十次免疫及之后,未检测到IgG2B自身抗体。根据这些结果推测,贫血是由IgG2B自身抗体引起的,而脾切除小鼠中出现的贫血突然加重是由于IgM自身抗体的产生。