The adaptor protein SLP-65 acts as a tumor suppressor that limits pre-B cell expansion
The adaptor protein SLP-65 acts as a tumor suppressor that limits pre-B cell expansion
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DOI：
10.1038/ni862
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发表时间：
2003-01-01
影响因子：
30.5
通讯作者：
Jumaa, H
中科院分区：
文献类型：
--
作者：
Flemming, A;Brummer, T;Jumaa, H
缺乏适配蛋白SLP-65(也称为BLNK)的小鼠成熟B细胞数量减少，但前B细胞隔间增加。我们在这里表明，与野生型细胞相比，SLP-65(-/-)前B细胞显示出增强的体外增殖能力。这种增殖需要白介素7和前B细胞受体(Pre-BCR)的表达。此外，SLP-65(-/-)小鼠的前B细胞淋巴瘤发病率很高。将SLP-65重新导入SLP-65(-/-)Pre-B细胞后，Pre-bcr表达下调，分化增强。我们的结果表明，SLP-65调节促进分化和限制前B细胞增殖的发育程序，从而发挥肿瘤抑制作用。
Mice deficient in the adaptor protein SLP-65 (also known as BLNK) have reduced numbers of mature B cells, but an increased pre-B cell compartment. We show here that compared to wild-type cells, SLP-65(-/-) pre-B cells show an enhanced ex vivo proliferative capacity. This proliferation requires interleukin 7 and expression of the pre-B cell receptor (pre-BCR). In addition, SLP-65(-/-) mice have a high incidence of pre-B cell lymphoma. Reintroduction of SLP-65 into SLP-65(-/-) pre-B cells led to preBCR down-regulation and enhanced differentiation. Our results indicate that SLP-65 regulates a developmental program that promotes differentiation and limits pre-B cell expansion, thereby acting as a tumor suppressor.