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
收藏
页码：12145 / 12150
页数：6
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