Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65

被引：264

作者：

Jumaa, H ^{[1
]}

Wollscheid, B ^{[1
]}

Mitterer, M ^{[1
]}

Wienands, J ^{[1
]}

Reth, M ^{[1
]}

Nielsen, PJ ^{[1
]}

机构：

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

来源：

IMMUNITY | 1999年 / 11卷 / 05期

关键词：

D O I：

10.1016/S1074-7613(00)80130-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP-65. We have investigated the role of SLP-65 in B cell maturation and function in mice deficient for SLP-65. While the mice are viable, B cell development is affected at several stages. SLP-65-deficient mice show increased proportions of pre-B cells in the bone marrow and immature B cells in peripheral lymphoid organs. B1 B cells are lacking. The mice show tower IgM and IgG3 serum titers and poor IgM but normal IgG immune responses. Mutant B cells show reduced Ca2+ mobilization and reduced proliferative responses to B cell mitogens. We conclude that white playing an important role, SLP-65 is not always required for signaling from the BCR.

引用

页码：547 / 554

页数：8

共 37 条

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