Hansen T H, Walsh W D, Ozato K, Arn J S, Sachs D H
J Immunol. 1981 Dec;127(6):2228-31.
Splenic B cells and B cell blasts from the I-A mutant mouse strain B6.C-H-2bm12 were tested by serology with a series of new monoclonal anti-Iab antibodies. Four out of 5 of those monoclonal antibody-defined specificities that are determined by wild-type I-Ab antigens were undetectable on B6.C-H-2bm12 cells. Specificities both present and absent on mutant cells appear to be determinants on the same wild-type molecule, as indicated by sequential precipitation experiments with soluble H-2b antigens. The lack of expression of certain Ia specificities on mutant cells was found not to be the result of disparate control by the Xid gene, which was previously shown to control the expression of Ia.W39, another specificity absent in B6.C-H-2bm12 mice. Serologic testing of Ia specificities on cells and blasts from F1-hybrid mice suggested that the Iabm12 antigens are codominantly expressed, indicating a failure to detect trans regulation or complementation of the mutant phenotype. Another monoclonal antibody-defined Ia specificity dependent on the expression of the E beta polypeptide was normally expressed in B6.C-H-2bm12 mice. These data thus suggest that the lesion of these mutant mice occurred in the A alpha and/or A beta structural gene, resulting in the loss of several Ia specificities.
用一系列新的单克隆抗Iab抗体通过血清学方法检测了I-A突变小鼠品系B6.C-H-2bm12的脾B细胞和B细胞母细胞。在野生型I-Ab抗原所决定的5种单克隆抗体定义的特异性中，有4种在B6.C-H-2bm12细胞上无法检测到。如用可溶性H-2b抗原进行的连续沉淀实验所示，突变细胞上存在和不存在的特异性似乎都是同一野生型分子上的决定簇。发现突变细胞上某些Ia特异性的缺失不是Xid基因不同调控的结果，Xid基因先前已被证明可控制Ia.W39的表达，W39是B6.C-H-2bm12小鼠中不存在的另一种特异性。对F1杂交小鼠的细胞和母细胞上Ia特异性的血清学检测表明，Iabm12抗原是共显性表达的，这表明未能检测到突变表型的反式调控或互补作用。另一种依赖于Eβ多肽表达的单克隆抗体定义的Ia特异性在B6.C-H-2bm12小鼠中正常表达。因此，这些数据表明这些突变小鼠的损伤发生在Aα和/或Aβ结构基因中，导致几种Ia特异性的丧失。
