Bcl11b is required for differentiation and survival of αβ T lymphocytes
Bcl11b is required for differentiation and survival of αβ T lymphocytes
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DOI：
10.1038/ni927
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发表时间：
2003-06-01
影响因子：
30.5
通讯作者：
Kominami, R
中科院分区：
文献类型：
--
作者：
Wakabayashi, Y;Watanabe, H;Kominami, R
编码锌指蛋白的基因Bcl 11b及其副产物Bcl 11 a与免疫系统恶性肿瘤有关。我们已经产生了Bcl 11 b缺陷小鼠，其在胸腺细胞发育的CD 4（-）CD 8（-）双阴性阶段显示出阻滞，而B-或γ δ T细胞谱系的细胞没有任何损伤。Bcl 11b（-/-）胸腺细胞显示V-β向D-β的不成功重组，并且由于缺乏Tcrb mRNA表达，细胞表面缺乏前T细胞受体（TCR）复合物。此外，我们还观察到新生Bcl 11b（-/-）小鼠胸腺中存在严重的细胞凋亡。这些结果表明，Bcl 11b是一个关键的调节分化和生存胸腺细胞发育过程中。
The gene Bcl11b, which encodes zinc finger proteins, and its paralog, Bcl11a, are associated with immune-system malignancies. We have generated Bcl11b-deficient mice that show a block at the CD4(-)CD8(-) double-negative stage of thymocyte development without any impairment in cells of B- or gammadelta T cell lineages. The Bcl11b(-/-) thymocytes showed unsuccessful recombination of V-beta to D-beta and lacked the pre-T cell receptor (TCR) complex on the cell surface, owing to the absence of Tcrb mRNA expression. In addition, we saw profound apoptosis in the thymus of neonatal Bcl11b(-/-) mice. These results suggest that Bcl11b is a key regulator of both differentiation and survival during thymocyte development.