Loss of precursor B cell expansion but not allelic exclusion in VpreB1/VpreB2 double-deficient mice.
Loss of precursor B cell expansion but not allelic exclusion in VpreB1/VpreB2 double-deficient mice.
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VPREB1/VPREB2双缺陷小鼠中前体B细胞扩张的损失，但不是等位基因排除。
DOI：
10.1084/jem.193.4.435
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发表时间：
2001-02-19
影响因子：
15.3
通讯作者：
Martensson, I L
中科院分区：
文献类型：
--
作者：
Mundt, C;Licence, S;Shimizu, T;Melchers, F;Martensson, I L
前 B 细胞受体由免疫球蛋白 (Ig) μ 重链和替代轻链（即 VpreB 和 λ5 蛋白）组成。为了分析两种 VpreB 蛋白的作用，生成了缺乏 VpreB1 和 VpreB2 基因的小鼠。 VpreB1 − /−VpreB2 − /− 小鼠在从 pre-BI 细胞转变为大 pre-BII 细胞时 B 细胞发育受损。 Pre-BII细胞不会通过增殖而扩增，因此骨髓中发现的小pre-BII和未成熟B细胞减少了40倍，并且脾脏中未成熟和成熟常规B细胞的生成似乎减少。此外，在腹膜中仅检测到少量的 B-1a 细胞。令人惊讶的是，Ig 重链等位排除仍然活跃，显然排除了包含 VpreB1/VpreB2 的受体在此过程中的信号传导作用。
The pre-B cell receptor consists of immunoglobulin (Ig) μ heavy chains and surrogate light chain, i.e., the VpreB and λ5 proteins. To analyze the role of the two VpreB proteins, mice lacking the VpreB1 and VpreB2 genes were generated. VpreB1 − /−VpreB2 − /− mice were impaired in their B cell development at the transition from pre-BI to large pre-BII cells. Pre-BII cells did not expand by proliferation, consequently 40-fold less small pre-BII and immature B cells were found in bone marrow, and the generation of immature and mature conventional B cells in spleen appeared reduced. In addition, only low numbers of B-1a cells were detected in the peritoneum. Surprisingly, Ig heavy chain allelic exclusion was still active, apparently ruling out a signaling role of a VpreB1/VpreB2–containing receptor in this process.