Delovitch T L, Sohn U
J Immunol. 1979 Apr;122(4):1528-34.
Allogeneic effect factors (AEF) were produced across an I-J subregion incompatibility. The helper activity of these AEFs is H-2 restricted since they help B cells only of the stimulator haplotype and of other haplotypes that carry the same I-J subregion gene(s) as the stimulator haplotype. Immunoadsorption studies demonstrate that they consist of I-J determinants derived initially from the GVHR host and MLR stimulator cells and not the GVHR donor and MLR responder cells used to generate AEF. It is postulated that the genetic restriction of AEF helper activity is mediated in part by the ability of the GVHR activated donor T cells to acquire, in vivo, recipient T cell and/or macrophage derived I-J determinants. Cellular adsorption studies indicate that AEF helper activity may be adsorbed by B cells, but neither T cells nor macrophages, of the stimulator haplotype. The results suggest that an I-J-positive AEF interacts with an I-J subregion controlled complementary recognition structure on a target B cell and, after antigenic stimulation, activates that B cell to IgG antibody synthesis.
同种异体效应因子(AEF)是在I-J亚区不相容的情况下产生的。这些AEF的辅助活性受H-2限制,因为它们仅辅助刺激单倍型以及携带与刺激单倍型相同I-J亚区基因的其他单倍型的B细胞。免疫吸附研究表明,它们由最初源自移植物抗宿主反应(GVHR)宿主和混合淋巴细胞反应(MLR)刺激细胞而非用于产生AEF的GVHR供体细胞和MLR反应细胞的I-J决定簇组成。据推测,AEF辅助活性的遗传限制部分是由GVHR激活的供体T细胞在体内获取受体T细胞和/或巨噬细胞衍生的I-J决定簇的能力介导 的。细胞吸附研究表明,AEF辅助活性可能被刺激单倍型的B细胞吸附,但不被T细胞或巨噬细胞吸附。结果表明,I-J阳性AEF与靶B细胞上I-J亚区控制的互补识别结构相互作用,并且在抗原刺激后,激活该B细胞进行IgG抗体合成。