Shinohara N, Hansen T H, Schurko E, McKenzie I F, Sachs D H
J Immunol. 1978 Dec;121(6):2472-6.
B10.AKM mice (H-2M) when immunized with H-2k cells showed very low cytotoxic antibody responses to the H-2Dk private specificity H-2.32, whereas AKR.M and (AKR.M X B10.AKM)F1 mice that possess the same H-2m haplotype mounted reasonable anti-H-2.32 antibody responses. The genetic nature of the non-H-2 linked gene(s) controlling the anti-H-2.32 response was analyzed on the backcross progeny raised between (AKR.M X B10.AKM)F1 and B10.AKM mice. The anti-H-2.32 antibody response was found to be predominantly controlled by a single locus. This locus segregated independently of the Ig heavy chain locus, the Ly2 locus, and the Mls locus. Despite the observed difference in antibody production, no significant differences between AKR.M and B10.AKM mice were detected in induction of H-2Dk-specific killer T cells. Thus, the defect in the response of B10.AKM mice to H-2.32 can be detected at the level of B cell function and is controlled by a single non-H-2-linked genetic locus, but is not attributable to genes linked to the major immunoglobulin structural genes nor to the Mls locus.
用H-2k细胞免疫的B10.AKM小鼠(H-2M)对H-2Dk私有特异性H-2.32表现出非常低的细胞毒性抗体反应,而具有相同H-2m单倍型的AKR.M和(AKR.M×B10.AKM)F1小鼠则产生了适度的抗H-2.32抗体反应。在(AKR.M×B10.AKM)F1和B10.AKM小鼠之间回交产生的后代中,分析了控制抗H-2.32反应的非H-2连锁基因的遗传性质。发现抗H-2.32抗体反应主要由一个基因座控制。该基因座与免疫球蛋白重链基因座、Ly2基因座和Mls基因座独立分离。尽管观察到抗体产生存在差异,但在诱导H-2Dk特异性杀伤性T细胞方面,未检测到AKR.M和B10.AKM小鼠之间存在显著差异。因此,B10.AKM小鼠对H-2.32反应的缺陷可在B细胞功能水平上检测到,且由一个单一的非H-2连锁遗传基因座控制,但不归因于与主要免疫球蛋白结构基因连锁的基因,也不归因于Mls基因座。