Pennycook J L, Chang Y, Celler J, Phillips R A, Wu G E
Department of Immunology, University of Toronto, Ontario, Canada.
J Exp Med. 1993 Sep 1;178(3):1007-16. doi: 10.1084/jem.178.3.1007.
The severe combined immunodeficiency (scid) mouse has a defective V(D)J recombinase activity that results in arrested lymphoid development at the pro-B cell stage in the B lineage. The defect is not absolute and scid mice do attempt gene rearrangement. Indeed, approximately 15% of all scid mice develop detectable levels of oligoclonal serum immunoglobulin and T cell activity. To gain more insight into the scid defect and its effect on V(D)J rearrangement, we analyzed DJH recombination in scid bone marrow. We determined that DJH structures are present in scid bone marrow and occur at a frequency only 10-100 times less than C.B-17+/+. The scid DJH repertoire is limited and resembles fetal liver DJH junctions, with few N insertions and predominant usage of reading frame 1. Moreover, 70% of the DJH structures were potentially productive, indicating that normal V(D)J recombinants should be arising continually.
严重联合免疫缺陷(scid)小鼠具有缺陷的V(D)J重组酶活性,这导致B淋巴细胞系在pro-B细胞阶段的淋巴细胞发育停滞。这种缺陷并非绝对,scid小鼠确实会尝试进行基因重排。实际上,所有scid小鼠中约有15%会产生可检测水平的寡克隆血清免疫球蛋白和T细胞活性。为了更深入了解scid缺陷及其对V(D)J重排的影响,我们分析了scid骨髓中的DJH重组。我们确定scid骨髓中存在DJH结构,其出现频率仅比C.B-17 +/+低10 - 100倍。scid DJH库有限,类似于胎肝DJH连接,N插入很少,且主要使用阅读框1。此外,70%的DJH结构可能具有功能性,这表明正常的V(D)J重组体应该会持续产生。