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

被引：153

作者：

Flemming, A

Brummer, T

Reth, M

Jumaa, H

机构：

[1] Univ Freiburg, Inst Biol 3, D-79108 Freiburg, Germany

[2] Max Planck Inst Immunbiol, D-79108 Freiburg, Germany

来源：

NATURE IMMUNOLOGY | 2003年 / 4卷 / 01期

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.

引用

页码：38 / 43

页数：6

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[1] B cell development: signal transduction by antigen receptors and their surrogates [J].