Analysis of the mechanism of production of pathologic autoantibodies

为了阐明多克隆B细胞的激活机制，我们首先利用固定化抗CD3的系统探索了活化的T细胞抑制B细胞的机制。虽然推测T细胞表面的CTLA4和B细胞表面的CD80/86之间的相互作用可能参与了这种抑制作用，但我们还没有得到直接的证据。我们还检测了固定化抗CD3刺激的丝裂霉素C处理的T细胞和B细胞是否会产生IgG型自身抗体。但未产生抗DNA、抗Sm、抗RNP的免疫球蛋白。单核细胞或α-干扰素也不能诱导免疫球蛋白M类抗DNA向免疫球蛋白类抗DNA的转化，其产生机制有待进一步研究。

In order to delineate the mechanism of polyclonal B cell activation, we first explore the mechanism of suppression of B cell by activated T cells using the system with immobilized anti-CD3. Although it was suggested that interactions between CTLA4 on T cells and CD80/86 on B cells might involve in the suppression, we could not get direct evidence.We also examined whether IgG type autoantibodies might be produced in cultures with immobilized anti-CD3 stimulated mitomycin C-treated T cells and B cells. However, none of IgG anti-DNA, anti-Sm, anti-RNP were produced. Nor could we induce class switch of IgM anti-DNA to IgG anti-DNA with monocytes or alpha-interferon.Further studies are required to investigate the mechanism of production of IgG anti-DNA.