The Journal of Experimental Medicine
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Published 25 February 2002. doi:10.1084/jem.20011751
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© Rockefeller University Press, 0022-1007/2002/3/535/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 5, March 4, 2002 535-545

Original Article

Essential Immunoregulatory Role for BCAP in B Cell Development and Function

Tetsuo Yamazaki1, Kiyoshi Takeda3, Kumiko Gotoh1,2, Hiroshi Takeshima4, Shizuo Akira3 and Tomohiro Kurosaki1,2

1 Department of Molecular Genetics, Institute for Liver Research, Kansai Medical University
2 Laboratory for Lymphocyte Differentiation, RIKEN Research Center for Allergy and Immunology, 10-15 Fumizono-cho, Moriguchi, Osaka 570-8506, Japan
3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan
4 Division of Cell Biology, Institute of Life Science, Kurume University, Kurume, Fukuoka 839-0861, Japan

Address correspondence to Tomohiro Kurosaki, Department of Molecular Genetics, Institute for Liver Research, 10-15 Fumizono-cho, Moriguchi, Osaka 570-8506, Japan. Phone: 81-6-6993-9445; Fax: 81-6-6994-6099; E-mail: kurosaki{at}mxr.mesh.ne.jp

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 Ca2+ mobilization and poor proliferative responses. These findings demonstrate that BCAP plays a pivotal immunoregulatory role in B cell development and humoral immune responses.

Key Words: mice • knockout • antigen receptor • phospholipase C-{gamma} • calcium


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