Lieber M R, Hesse J E, Lewis S, Bosma G C, Rosenberg N, Mizuuchi K, Bosma M J, Gellert M
Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892.
Cell. 1988 Oct 7;55(1):7-16. doi: 10.1016/0092-8674(88)90004-9.
Pre-B and pre-T cell lines from mutant mice with severe combined immune deficiency (scid mice) were transfected with plasmids that contained recombination signal sequences of antigen receptor gene elements (V, D, and J). Recovered plasmids were tested for possible recombination of signal sequences and/or the adjacent (coding) sequences. Signal ends were joined, but recombination was abnormal in that half of the recombinants had lost nucleotides from one or both signals. Coding ends were not joined at all in either deletional or inversional V(D)J recombination reactions. However, coding ends were able to participate in alternative reactions. The failure of coding joint formation in scid pre-B and pre-T cells appears sufficient to explain the absence of immunoglobulin or T cell receptor production in scid mice.
将含有抗原受体基因元件（V、D和J）重组信号序列的质粒转染到患有严重联合免疫缺陷的突变小鼠（scid小鼠）的前B细胞系和前T细胞系中。对回收的质粒进行信号序列和/或相邻（编码）序列可能重组的检测。信号末端发生连接，但重组异常，因为一半的重组体在一个或两个信号中丢失了核苷酸。在缺失或倒位的V(D)J重组反应中，编码末端根本没有连接。然而，编码末端能够参与其他反应。scid前B细胞和前T细胞中编码连接形成的失败似乎足以解释scid小鼠中免疫球蛋白或T细胞受体产生的缺失。
