Essential immunoregulatory role for BCAP in B cell development and function

被引:100
作者
Yamazaki, T
Takeda, K
Gotoh, K
Takeshima, H
Akira, S
Kurosaki, T
机构
[1] Kansai Med Univ, Dept Mol Genet, Inst Liver Res, Moriguchi, Osaka 5708506, Japan
[2] Kansai Med Univ, RIKEN, Res Ctr Allergy & Immunol, Lab Lymphocyte Differentiat, Moriguchi, Osaka 5708506, Japan
[3] Osaka Univ, Dept Host Def, Microbial Dis Res Inst, Suita, Osaka 5650871, Japan
[4] Kurume Univ, Inst Life Sci, Div Cell Biol, Fukuoka 8390861, Japan
关键词
mice; knockout; antigen receptor; phospholipase C-gamma; calcium;
D O I
10.1084/jem.20011751
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
BCAP was recently cloned as a binding molecule to phosphoinositide 3-kinase (PI3K). To investigate the role of BCAP, mutant mice deficient in BCAP were generated. While BCAP-deficient mice are viable, they have decreased numbers of mature B cells and B1 B cell deficiency. The mice produce lower titers of serum immunoglobulin (Ig)M and IgG3, and mount attenuated responses to T cell-independent type II antigen. Upon B cell receptor cross-linking, BCAP-deficient B cells exhibit reduced Ca(2+) mobilization and poor proliferative responses. These findings demonstrate that BCAP plays a pivotal immunoregulatory role in B cell development and humoral immune responses.
引用
收藏
页码:535 / 545
页数:11
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