Bitoh S, Fujimoto S, Yamamoto H
Department of Immunology, Kochi Medical School, Japan.
Immunology. 1989 Apr;66(4):479-84.
We have previously reported that the immunization of BALB/c mice with MOPC-104E myeloma protein (M104E) induced idiotype-specific Ly 1-negative B lymphocytes that had an ability to enhance idiotype-positive anti-dextran antibody production. It was also shown that the cell interaction between idiotypic and anti-idiotypic B lymphocytes was observed in a class II-restricted manner. The effect of monoclonal anti-class II antibody on the B-B cell interaction is investigated in this report. The addition of anti-I-A or anti-I-E monoclonal antibody into the B-B cell interaction system, from both BALB/c (H-2d) and BALB.K (H-2k), inhibited the enhanced antibody production mediated by idiotype-immune B lymphocytes. Interestingly, however, it was revealed that the anti-I-A and anti-I-E antibodies acted differently on each B-lymphocyte population. Pretreatment of an anti-idiotypic (idiotype-immune) enhancing B-lymphocyte population with anti-I-A antibody diminished its enhancing activity, while anti-I-E did not. On the other hand, pretreatment of dextran-immune antibody producing B cells with anti-I-A antibody showed no effect, while anti-I-E inhibited anti-dextran antibody production. When the enhancing B-lymphocyte population of F1 mice was treated with anti-I-A antibody specific for one of their parents' haplotypes, co-operation with the respective haplotype B cells was inhibited, but the other haplotype was not. The inhibitory effect of anti-class II antibodies could only be seen at the early phase of culture period. Taken together, the results of these experiments suggest that the class II antigens are concerned with the self-recognitive cell interaction among B lymphocytes in the frame of idiotype network systems.
我们先前曾报道,用MOPC-104E骨髓瘤蛋白(M104E)免疫BALB/c小鼠可诱导独特型特异性Ly 1阴性B淋巴细胞,该细胞具有增强独特型阳性抗右旋糖酐抗体产生的能力。还表明独特型和抗独特型B淋巴细胞之间的细胞相互作用是以II类限制的方式观察到的。本报告研究了单克隆抗II类抗体对B - B细胞相互作用的影响。将抗I - A或抗I - E单克隆抗体添加到来自BALB/c(H - 2d)和BALB.K(H - 2k)的B - B细胞相互作用系统中,可抑制由独特型免疫B淋巴细胞介导的抗体产生增强。然而,有趣的是,发现抗I - A和抗I - E抗体对每个B淋巴细胞群体的作用不同。用抗I - A抗体预处理抗独特型(独特型免疫)增强B淋巴细胞群体可降低其增强活性,而抗I - E则无此作用。另一方面,用抗I - A抗体预处理产生右旋糖酐免疫抗体的B细胞没有效果,而抗I - E则抑制抗右旋糖酐抗体的产生。当用针对其亲本单倍型之一的抗I - A抗体处理F1小鼠的增强B淋巴细胞群体时,与相应单倍型B细胞的合作受到抑制,但另一个单倍型不受影响。抗II类抗体的抑制作用仅在培养期的早期可见。综上所述,这些实验结果表明II类抗原在独特型网络系统框架内与B淋巴细胞之间的自身识别细胞相互作用有关。