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The adaptor protein SLP-65 acts as a tumor suppressor that limits pre-B cell expansion
被引:153
作者:

Flemming, A
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机构: Univ Freiburg, Inst Biol 3, D-79108 Freiburg, Germany

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Reth, M
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机构: Univ Freiburg, Inst Biol 3, D-79108 Freiburg, Germany

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机构:
[1] Univ Freiburg, Inst Biol 3, D-79108 Freiburg, Germany
[2] Max Planck Inst Immunbiol, D-79108 Freiburg, Germany
关键词:
D O I:
10.1038/ni862
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
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.
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页码:38 / 43
页数:6
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