Continued RAG expression in late stages of B cell development and no apparent re-induction after immunization
Continued RAG expression in late stages of B cell development and no apparent re-induction after immunization
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DOI：
10.1038/23287
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发表时间：
1999-08-12
期刊：
影响因子：
64.8
通讯作者：
Nussenzweig, MC
中科院分区：
文献类型：
--
作者：
Yu, W;Nagaoka, H;Nussenzweig, MC
免疫系统中的B细胞发育模型表明，只有骨髓中接受受体编辑的未成熟B细胞表达V(D) j -重组激活基因（RAGs）（1-3）。在这里，我们研究了在携带编码绿色荧光的细菌人工染色体的转基因小鼠中RAG表达的调控。而不是RAG2（参考文献4）。我们发现报告基因在骨髓和脾脏的所有未成熟B细胞中表达。内源性RAG信使RNA在骨髓和脾脏的未成熟蜂鸟中表达，并随着它们获得更高水平的表面免疫球蛋白M （IgM）而降低两个数量级。一旦RAG表达停止，在免疫应答过程中就不会再被诱导。我们的发现可能有助于调和一系列明显矛盾的观察结果，并为调节等位基因排斥、受体编辑和耐受性的机制提供了一个新的模型。
Models of B-cell-development in the immune system suggest that only those immature B cells in the bone marrow that undergo receptor editing express V(D)J-recombination-activating genes (RAGs)(1-3). Here we investigate the regulation of RAG expression in transgenic mice carrying a bacterial artificial chromosome that encodes a green fluorescent. protein reporter instead of RAG2 (ref. 4). We find that the reporter is expressed in all immature B cells in the bone marrow and spleen. Endogenous RAG messenger RNA is expressed in immature beeps in bone marrow and spleen and decreases by two orders of magnitude as they acquire higher levels of surface immunoglobulin M (IgM). Once RAG expression is stopped it is not re-induced during immune responses. Our findings may help to reconcile a series of apparently contradictory observations, and suggest a new model for the mechanisms that regulate allelic exclusion, receptor editing and tolerance.