The B-cell antigen receptor integrates adaptive and innate immune signals

被引：31

作者：

Otipoby, Kevin L. ^{[1
]}

Waisman, Ari ^{[2
]}

Derudder, Emmanuel ^{[1
,3
]}

Srinivasan, Lakshmi ^{[1
]}

Franklin, Andrew ^{[3
]}

Rajewsky, Klaus ^{[1
,2
,3
]}

机构：

[1] Harvard Univ, Sch Med, Immune Dis Inst, Boston, MA 02115 USA

[2] Univ Cologne, Inst Genet, D-50674 Cologne, Germany

[3] Max Delbruck Ctr Mol Med, Lab Immune Regulat & Canc, D-13125 Berlin, Germany

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2015年 / 112卷 / 39期

基金：

欧盟地平线“2020”; 欧洲研究理事会; 美国国家卫生研究院;

关键词：

BCR; B-cell proliferation; PI-3K; GSK3; beta; Foxo1; MOUSE IMMUNOGLOBULIN ANTIBODIES; LYMPHOCYTE DEVELOPMENT; KAPPA-B; GENE; ACTIVATION; KINASE; EXPRESSION; RESPONSES; SURVIVAL; PATHWAY;

D O I：

10.1073/pnas.1516428112

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

B cells respond to antigens by engagement of their B-cell antigen receptor (BCR) and of coreceptors through which signals from helper T cells or pathogen-associated molecular patterns are delivered. We show that the proliferative response of B cells to the latter stimuli is controlled by BCR-dependent activation of phosphoinositidyl 3-kinase (PI-3K) signaling. Glycogen synthase kinase 3 beta and Foxo1 are two PI-3K-regulated targets that play important roles, but to different extents, depending on the specific mitogen. These results suggest a model for integrating signals from the innate and the adaptive immune systems in the control of the B-cell immune response.

引用

页码：12145 / 12150

页数：6

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