DEVELOPMENT OF B-CELLS IN SCID MICE WITH IMMUNOGLOBULIN TRANSGENES - IMPLICATIONS FOR THE CONTROL OF V(D)J RECOMBINATION
DEVELOPMENT OF B-CELLS IN SCID MICE WITH IMMUNOGLOBULIN TRANSGENES - IMPLICATIONS FOR THE CONTROL OF V(D)J RECOMBINATION
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DOI：
10.1016/1074-7613(95)90005-5
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发表时间：
1995-06-01
期刊：
影响因子：
32.4
通讯作者：
BOSMA, MJ
中科院分区：
文献类型：
--
作者：
CHANG, Y;BOSMA, GC;BOSMA, MJ
scid原B细胞不能进展到前B和B细胞阶段被认为是由缺陷的重组酶活性引起的，该重组酶活性不能解决由尝试的V（D）J重组引起的染色体断裂。为了支持这一模型，我们报道了某些免疫球蛋白转基因，特别是那些在野生型小鼠中强烈抑制内源性V-H-to-DJ（H）和V κ-to-J κ重排的转基因，允许scid pro-B细胞进展到前B和B细胞阶段。scid B细胞分化的这种拯救与重组激活基因RAG 1和RAG 2的表达的显著降低以及κ基因座的转录降低有关。
The inability of scid pro-B cells to progress to the pre-B and B cell stages is believed to be caused by a defective recombinase activity that fails to resolve chromosomal breaks resulting from attempted V(D)J recombination. In support of this model, we report that certain immunoglobulin transgenes, specifically those which strongly inhibit endogenous V-H-to-DJ(H) and V kappa-to-J kappa rearrangement in wild-type mice, allow scid pro-B cells to progress to the pre-B and B cell stages. this rescue of scid B cell differentiation is associated with a dramatic reduction in expression of the recombination activation genes, RAG1 and RAG2, and with reduced transcription of the kappa locus.