A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

被引：372

作者：

Clayton, E

Bardi, G

Bell, SE

Chantry, D

Downes, CP

Gray, A

Humphries, LA

Rawlings, D

Reynolds, H

Vigorito, E

Turner, M ^{[1
]}

机构：

[1] Babraham Inst, Mol Immunol Programme, Lab Lymphocyte Signaling & Dev, Cambridge CB2 4AT, England

[2] COS Corp, Bothell, WA 98021 USA

[3] Univ Dundee, Dept Biochem, Dundee DD1 5EH, Scotland

[4] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA

[5] Univ Washington, Sch Med, Dept Immunol, Seattle, WA 98195 USA

[6] Univ Washington, Sch Med, Dept Pediat, Seattle, WA 98195 USA

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2002年 / 196卷 / 06期

关键词：

Akt; Btk; calcium; gone targeting; p110; delta;

D O I：

10.1084/jem.20020805

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 lacking the p 1108 catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110delta(-/-) B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110delta function is required for BCR-mediated calcium flux, activation of phosphipaseCgamma2, and Bruton's tyrosine kinase. Thus, p110delta plays a critical role in B cell homeostasis and function.

引用

收藏

页码：753 / 763

页数：11

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