Kaplan R B, Quintáns J
J Exp Med. 1979 Jan 1;149(1):267-72. doi: 10.1084/jem.149.1.267.
F1 male mice with the CBA/N X-linked defect that are unable to produce plaque-forming cell responses to phosphorylcholine (PC) provide normal PC-specific helper T-cell activity when compared to F1 female littermates. Inhibition of helper activity with anti-idiotypic antiserum indicates that PC-specific T cells from both NBF1 female and male mice possess predominantly BALB/c myeloma protein HOPC-8 idiotypic determinants. Therefore, the CBA/N defect cannot be explained as a deletion of genes coding for V-region anti-PC specificities. The demonstration of helper activity in NBF1 male mice, which occurs in the absence of anti-PC antibody synthesis, also demonstrates the endogenous origin of the T-cell receptor.
具有CBA/N X连锁缺陷的F1雄性小鼠不能对磷酸胆碱(PC)产生噬斑形成细胞反应,与同窝F1雌性小鼠相比,其提供正常的PC特异性辅助性T细胞活性。用抗独特型抗血清抑制辅助活性表明,来自NBF1雌性和雄性小鼠的PC特异性T细胞主要具有BALB/c骨髓瘤蛋白HOPC-8独特型决定簇。因此,CBA/N缺陷不能解释为编码V区抗PC特异性的基因缺失。在不合成抗PC抗体的情况下,NBF1雄性小鼠中辅助活性的证明也证明了T细胞受体的内源性起源。