Brunati S, Moncuit J, Fridman W H, Teillaud J L
Unité INSERM 255, Institut Curie, Paris, France.
Eur J Immunol. 1990 Jan;20(1):55-61. doi: 10.1002/eji.1830200109.
In this work, we analyzed the immunoglobulin heavy (H) and light (L) chain production by two variant B hybridomas, UN2.C3 and UN2.C17.K1 co-cultured with cells from a Fc gamma RII+, IgG-binding factor (IgG-BF)-producer T hybridoma (T2D4.C1) or with cells of a Fc gamma RII-, IgG-BF-nonproducer variant (D10C5). We showed that only the Fc gamma RII+ hybridoma directly inhibits the IgG secretion by UN2.C3 through a soluble mediator. This inhibition affects the H and L chain synthesis as well as the H and L chain-encoding mRNA steady state. No apparent cytotoxic effect could be detected. In contrast, the production of kappa chain by an H chain-negative variant (UN2.C17.K1) was unaffected. This indicates that a complete IgG molecule is required to observe the inhibitory effect induced by T2D4.C1. The pattern of effector/target cell interactions observed in our work suggests that the soluble factor involved in the suppression of IgG production is IgG-BF, able to transiently modify the IgG gene expression in target cells.
在本研究中,我们分析了两种变异B杂交瘤UN2.C3和UN2.C17.K1与来自FcγRII +、产生IgG结合因子(IgG - BF)的T杂交瘤(T2D4.C1)的细胞或与FcγRII -、不产生IgG - BF的变异体(D10C5)的细胞共培养时免疫球蛋白重链(H)和轻链(L)的产生情况。我们发现,只有FcγRII +杂交瘤通过一种可溶性介质直接抑制UN2.C3的IgG分泌。这种抑制作用影响H链和L链的合成以及H链和L链编码mRNA的稳态。未检测到明显的细胞毒性作用。相比之下,H链阴性变异体(UN2.C17.K1)的κ链产生不受影响。这表明需要完整的IgG分子才能观察到T2D4.C1诱导的抑制作用。我们研究中观察到的效应细胞/靶细胞相互作用模式表明,参与抑制IgG产生的可溶性因子是IgG - BF,它能够瞬时改变靶细胞中IgG基因的表达。